Compositions and methods for treating myelodysplastic syndromes (MDS)

Abstract

Aspects of the disclosure provides composition and methods for treating a subject having MDS, the method comprising administering to the subject a hemojuvelin (HIV) antagonist (e.g., anti-HJV antibody).

Description

COMPOSITIONS AND METHODS FOR TREATING MYELODYSPLASTIC SYNDROMES (MDS) RELATED APPLICATION

[0001] This application claims the benefit under 35 U.S.C. § 119(e) of US Provisional Application No. 63 / 651,706, filed May 24, 2024, entitled “COMPOSITIONS AND METHODS FOR TREATING MYELODYSPLASTIC SYNDROMES (MDS)” the content of which is hereby incorporated by reference herein in its entirety for all purposes. REFERENCE TO AN ELECTRONIC SEQUENCE LISTING

[0002] The contents of the electronic sequence listing (D084270016WO00-SEQ-VLJ.xml; Size: 153,887 bytes; and Date of Creation: May 21, 2025) are herein incorporated by reference in its entirety. BACKGROUND

[0003] Anemia, a major clinical manifestation in MDS, is present in large percentage of MDS patients when the disease is first diagnosed. Patients with MDS associated anemia are often resistant to conventional therapeutic agents for treating anemia. SUMMARY

[0004] The disclosure, at least in part, provides compositions and methods for treating a subject having MDS, the method comprising administering to the subject a hemojuvelin (HJV) antagonist (e.g., anti-HJV antibody). In some aspects, the disclosure provides a method of treating myelodysplastic syndrome (MDS) comprising administering an anti-HJV antibody to a functionally iron deficient subject having MDS. In some aspects, the disclosure provides a method of treating myelodysplastic syndrome (MDS) comprising administering an anti-HJV antibody to a subject having MDS, wherein the subject has elevated hepcidin levels. In some embodiments, the subject with MDS is functionally iron deficient, and the administration results in release of cellular iron stores. In some embodiments, administration of an anti-HJV antibody results in release of cellular iron stores in the amount sufficient to treat anemia in the subject (e.g., a functionally iron deficient subject having MDS).

[0005] In some aspects, the present disclosure provides a method for administering an anti- HJV antibody to a functionally iron deficient subject having myelodysplastic syndrome (MDS).

[0006] In some aspects, the present disclosure provides a method comprising administering an anti-HJV antibody to a subjecting having myelodysplastic syndrome (MDS), wherein the subject has an elevated hepcidin level.

[0007] In some aspects, the present disclosure relates to methods of treating MDS in a subject having or at risk of having MDS by administering to the subject a hemojuvelin (HJV) antagonist (e.g., anti-HJV antibody).

[0008] In some aspects, methods of treating MDS comprise administering an anti-HJV antibody to a functionally iron deficient subject having MDS. In some embodiments, the administration results in release of cellular iron stores.

[0009] In some aspects, methods of treating MDS comprise administering an anti-HJV antibody to an anemic subject having MDS. In some embodiments, administration of an anti- HJV antibody results in release of cellular iron stores in the amount sufficient to treat anemia in the subject (e.g., a functionally iron deficient subject having MDS).

[0010] In some aspects, methods of treating MDS comprise administering an anti- HJV antibody to a subject having MDS, wherein the subject has elevated hepcidin levels. In some embodiments, administration of an anti-HJV antibody results in a reduction of hepcidin levels.

[0011] In some aspects, methods of treating MDS comprise administering an anti- HJV antibody to a subject having very low to moderate low MDS in a subject. In some embodiments, administration of an anti-HJV antibody to a subject results in release of cellular iron stores. In some embodiments, administration of an anti-HJV antibody to the a subject results in release of cellular iron stores in the amount sufficient to treat anemia in the subject.

[0012] In some embodiments, the subject has low to moderate low MDS according to International Prognostic Scoring System (IPSS) Revised (IPSS-R). In some embodiments, the subject has very low MDS according to International Prognostic Scoring System (IPSS) Molecular (IPSS-M). In some embodiments, the subject has an IPSS-M risk score of less than -1.5. In some embodiments, the subject has low MDS according to IPSS-M. In some embodiments, the subject has an IPSS-M risk score in the range of -1.5 to -0.5. In some embodiments, the subject has moderate low MDS according to IPSS-M. In some embodiments, the subject has an IPSS-M risk score in the range of -0.5 to 0. In someembodiments, the subject has moderate high MDS according to IPSS-M. In some embodiments, the subject has an IPSS-M risk score in the range of 0 to 0.5.

[0013] In some embodiments, the subject has MDS / myeloproliferative neoplasm (MPN) (MDS / MPN). In some embodiments, the subject does not have MDS / MPN with ring sideroblasts. In some embodiments, the MDS / MPN is MDS / MPN with ring sideroblasts and thrombocytosis (RS-T) (MDS / MPN with RS-T). In some embodiments, a subject described herein does not have MDS / MPN is MDS / MPN with ring sideroblasts and thrombocytosis (RS-T) (MDS / MPN with RS-T). In some embodiments, the MDS / MPN is chronic myelomonocytic leukemia (CMML). In some embodiments, the subject does not have secondary MDS. In some embodiments, the subject has Del(5q) MDS. In some embodiments, the subject has elevated hepcidin levels.

[0014] In some embodiments, the subject has refractory anemia (RA). In some embodiments, the subject has MDS with excess blasts (MDS-EB). In some embodiments, the subject has MDS with excess blasts (MDS-EB). In some embodiments, the subject has MDS with ringed sideroblasts (MDS-RS). In some embodiments, the subject has MDS with single lineage dysplasia (MDS-SLD). In some embodiments, the subject has MDS with multilineage dysplasia (MDS-MLD).

[0015] In some embodiments, the subject has less than 10% blast cells in the bone marrow. In some embodiments, the subject has 5-10% blast cells in the bone marrow. In some embodiments, the subject has less than 5% blast cells in the bone marrow. In some embodiments, the subject has less than 5% circulating blast cells.

[0016] In some embodiments, the subject comprises one or more mutations in TET2, ASXL1, NRAS, JAK2, CBL, IDH2, NPM1, IDH1, KRAS, GNAS, PTPN11, BRAF, PTEN, and / or CDKN2A.

[0017] In some embodiments, the subject has a baseline hemoglobin level of less than 10 g / dL. In some embodiments, the subject has a baseline serum ferritin level of at least 30 µg / L. In some embodiments, the subject has a baseline platelet count in the range of 25,000- 1,000,000 / µL. In some embodiments, the subject has a baseline total white blood cell count of less than 50,000 / µL. In some embodiments, the subject has a transferrin saturation (TSAT) level of less than 75%.

[0018] In some embodiments, the subject has a baseline level of aspartate aminotransferase (AST) of less than 3.0x upper limit of normal (ULN). In some embodiments, the subject has a baseline level of alanine transaminase (ALT) of <3.0x ULN.In some embodiments, the subject has a baseline level of direct bilirubin of <2.0x ULN. In some embodiments, the subject has an estimated glomerular filtration rate (eGFR) of at least 30mL / min / 1.73m2.

[0019] In some embodiments, the subject has an Eastern Cooperative Oncology Group (ECOG) performance score of less than 2.

[0020] In some embodiments, the subject does not have vitamin B12 deficiency. In some embodiments, the subject does not have folate deficiency. In some embodiments, the subject does not have an infection.

[0021] In some embodiments, the subject does not have neutropenia. In some embodiments, the subject does not have thrombocytopenia. In some embodiments, the subject does not have acute myeloid leukemia (AML). In some embodiments, the subject does not have hereditary hemochromatosis. In some embodiments, the subject does not have a hemoglobinopathy associated with anemia. In some embodiments, the subject does not have an intrinsic red blood cell defect associated with anemia. In some embodiments, the subject does not have active immune-mediated hemolytic anemia. In some embodiments, the subject does not have non-surgical bleeding causing a decrease in hemoglobin of more than 2g / dL.

[0022] In some embodiments, the subject has received no more than 2 units of red blood cell transfusion 6 months prior to administration of the anti-HJV antibody to the subject. In some embodiments, the subject has received no more than 12 units of red blood cell transfusion for MDS related anemia. In some embodiments, the subject has not received a hematopoietic cell transplant within 10 years of the administration of the anti-HJV antibody. In some embodiments, the subject has not received iron chelation therapy within 28 days of the administration of the anti-HJV antibody.

[0023] In some embodiments, the subject has not received a total splenectomy. In some embodiments, the subject has not received major surgery within 8 weeks of the administration of the anti-HJV antibody.

[0024] In some embodiments, the subject has not been diagnosed with a malignancy within 3 years of the administration of the anti-HJV antibody to the subject. In some embodiments, the subject has not received anemia directed therapies within 28 days of the administration of the anti-HJV antibody.

[0025] In some embodiments, the subject has received MDS treatment prior to the administration of the anti-HJV antibody.

[0026] In some embodiments, the method of treating MDS comprises administering an anti-HJV antibody to a subject having MDS and further comprises administering atherapeutic agent for treating MDS to the subject. In some embodiments, the anti-HJV antibody and the therapeutic agent for treating MDS are administered concomitantly. In some embodiments, the anti-HJV antibody and the therapeutic agent for treating MDS are administered sequentially. In some embodiments, the anti-HJV antibody and the therapeutic agent for treating MDS are administered at different frequencies.

[0027] In some embodiments, the therapeutic agent for treating MDS is for iron chelation. In some embodiments, the therapeutic agent for treating MDS is a growth factor. In some embodiments, the therapeutic agent for treating MDS is luspatercept. In some embodiments, the therapeutic agent for treating MDS is lenalidomide. In some embodiments, the therapeutic agent for treating MDS is an immune modulator. In some embodiments, the therapeutic agent for treating MDS is allogeneic stem cell transplantation. In some embodiments, the therapeutic agent for treating MDS is a hypomethylating agent (HMA).

[0028] In some embodiments, the anti-HJV antibody is administered intravenously or subcutaneously.

[0029] In some embodiments, the antibody comprises a HC CDR1 comprising the amino acid of SEQ ID NO: 1, a HC CDR2 comprising the amino acid of SEQ ID NO: 2, a HC CDR3 comprising the amino acid of SEQ ID NO: 3; an LC CDR1 comprising the amino acid of SEQ ID NO: 17, a LC CDR2 comprising the amino acid of SEQ ID NO: 5, and a LC CDR3 comprising the amino acid of SEQ ID NO: 27.

[0030] In some embodiments, the anti-HJV antibody comprises a VH comprising the amino acid sequence of SEQ ID NO: 38, and a VL comprising the amino acid sequence of SEQ ID NO: 39.

[0031] In some embodiments, the anti-HJV antibody comprises a heavy chain comprising the amino acid sequence of SEQ ID NO: 61, and a light chain comprising the amino acid sequence of SEQ ID NO: 62.

[0032] In some embodiments, the anti-HJV antibody comprises a heavy chain comprising the amino acid sequence of SEQ ID NO: 63, and a light chain comprising the amino acid sequence of SEQ ID NO: 62.

[0033] In some embodiments, the administration of an anti-HJV antibody increases hemoglobin level in the subject. In some embodiments, the administration of an anti-HJV antibody increases hemoglobin level in the subject by at least 1 g / dL.

[0034] In some embodiments, the administration of an anti-HJV antibody increases TSAT% in the subject relative to the TSAT% prior to administration. In some embodiments, the administration of an anti-HJV antibody increases TSAT% in the subject by between 10%and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, or between 10% and 15%, relative to the TSAT% prior to administration.

[0035] In some embodiments, the administration of an anti-HJV antibody decreases circulating hepcidin level in the subject relative to the circulating hepcidin level prior to administration. In some embodiments, the administration of an anti-HJV antibody decreases circulating hepcidin level in the subject by between 5% and 30%, between 5% and 20%, or between 5% and 15%, relative to the circulating hepcidin level prior to administration.

[0036] In some embodiments, the administration of an anti-HJV antibody increases serum iron level in the subject compared to before administration.

[0037] In some embodiments, the administration of an anti-HJV antibody increases mean corpuscular hemoglobin in the subject compared to before administration.

[0038] In some embodiments, the administration of an anti-HJV antibody increases mean corpuscular hemoglobin concentration in the subject compared to before administration. BRIEF DESCRIPTION OF THE DRAWINGS

[0039] The accompanying drawings, which are incorporated in and constitute a part of this specification, illustrate certain embodiments, and together with the written description, serve to provide non-limiting examples of certain aspects of the compositions and methods disclosed herein.

[0040] FIG. 1 is a graph showing an anti-HJV mAb decreased serum hepcidin level at 5 mg / kg or 20 mg / kg in MDS mice (***p < 0.01 vs Vehicle group; one-way ANOVA).

[0041] FIGs. 2A-2B are graphs showing anti-HJV mAb increased serum iron (FIG. 2A) and transferrin saturation (TSAT) (FIG. 2B) at 5 mg / kg or 20 mg / kg in MDS mice (***p < 0.001 vs Vehicle group; one-way ANOVA).

[0042] FIG. 3 is a graph showing an anti-HJV mAb increased HGB level at 5 mg / kg or 20 mg / kg in MDS mice (* p < 0.05, **p < 0.01 vs Vehicle group; one-way ANOVA).

[0043] FIGs. 4A-4B are graphs showing anti-HJV mAb increased MCH (FIG. 4A) and MCHC (FIG. 4B) at 5 mg / kg or 20 mg / kg in MDS mice (**p < 0.01 vs Vehicle group; one-way ANOVA).

[0044] FIGs. 5A-5C are graphs showing anti-HJV mAb did not affect red blood cell (RBC) count (FIG. 5A), white blood cells (WBC) (FIG. 5B), and / or platelet level (vs vehicle) (FIG. 5C) in MDS mice.DETAILED DESCRIPTION

[0045] The disclosure, at least in part, provides compositions and methods for treating a subject having MDS, the method comprising administering to the subject a hemojuvelin (HJV) antagonist (e.g., anti-HJV antibody). In some embodiments, the subject with MDS is functionally iron deficient, and the administration results in release of cellular iron stores. In some embodiments, administration of an anti-HJV antibody results in release of cellular iron stores in the amount sufficient to treat anemia in the subject (e.g., a functionally iron deficient subject having MDS).

[0046] Further aspects of the disclosure, including a description of defined terms, are provided below. I. Definitions

[0047] Administering: As used herein, the terms “administering” or “administration” means to provide a complex to a subject in a manner that is physiologically and / or pharmacologically useful (e.g., to treat a condition in the subject).

[0048] Antibody: As used herein, the term “antibody” refers to a polypeptide that includes at least one immunoglobulin variable domain or at least one antigenic determinant, e.g., paratope that specifically binds to an antigen. In some embodiments, an antibody is a full- length antibody. In some embodiments, an antibody is a chimeric antibody. In some embodiments, an antibody is a humanized antibody. However, in some embodiments, an antibody is a Fab fragment, a F(ab')2 fragment, a Fv fragment or a scFv fragment. In some embodiments, an antibody is a nanobody derived from a camelid antibody or a nanobody derived from shark antibody. In some embodiments, an antibody is a diabody. In some embodiments, an antibody comprises a framework having a human germline sequence. In another embodiment, an antibody comprises a heavy chain constant domain selected from the group consisting of IgG, IgG1, IgG2, IgG2A, IgG2B, IgG2C, IgG3, IgG4, IgA1, IgA2, IgD, IgM, and IgE constant domains. In some embodiments, an antibody comprises a heavy (H) chain variable region (abbreviated herein as VH), and / or a light (L) chain variable region (abbreviated herein as VL). In some embodiments, an antibody comprises a constant domain, e.g., an Fc region. An immunoglobulin constant domain refers to a heavy or light chain constant domain. Human IgG heavy chain and light chain constant domain amino acid sequences and their functional variations are known. With respect to the heavy chain, in some embodiments, the heavy chain of an antibody described herein can be an alpha (α), delta (∆),epsilon (ε), gamma (γ) or mu (µ) heavy chain. In some embodiments, the heavy chain of an antibody described herein can comprise a human alpha (α), delta (∆), epsilon (ε), gamma (γ) or mu (µ) heavy chain. In a particular embodiment, an antibody described herein comprises a human gamma 1 CH1, CH2, and / or CH3 domain. In some embodiments, the amino acid sequence of the VH domain comprises the amino acid sequence of a human gamma (γ) heavy chain constant region, such as any known in the art. Non-limiting examples of human constant region sequences have been described in the art, e.g., see U.S. Pat. No. 5,693,780 and Kabat E A et al., (1991) supra . In some embodiments, the VH domain comprises an amino acid sequence that is at least 70%, 75%, 80%, 85%, 90%, 95%, 98%, or at least 99% identical to any of the variable chain constant regions provided herein. In some embodiments, an antibody is modified, e.g., modified via glycosylation, phosphorylation, sumoylation, and / or methylation. In some embodiments, an antibody is a glycosylated antibody, which is conjugated to one or more sugar or carbohydrate molecules . In some embodiments, the one or more sugar or carbohydrate molecule are conjugated to the antibody via N-glycosylation, O-glycosylation, C-glycosylation, glypiation (GPI anchor attachment), and / or phosphoglycosylation. In some embodiments, the one or more sugar or carbohydrate molecule are monosaccharides, disaccharides, oligosaccharides, or glycans . In some embodiments, the one or more sugar or carbohydrate molecule is a branched oligosaccharide or a branched glycan. In some embodiments, the one or more sugar or carbohydrate molecule includes a mannose unit, a glucose unit, an N-acetylglucosamine unit, or a phospholipid unit. In some embodiments, an antibody is a construct that comprises a polypeptide comprising one or more antigen binding fragments of the disclosure linked to a linker polypeptide or an immunoglobulin constant domain. Linker polypeptides comprise two or more amino acid residues joined by peptide bonds and are used to link one or more antigen binding portions. Examples of linker polypeptides have been reported (see e.g., Holliger, P., et al. (1993) Proc. Natl. Acad. Sci. USA 90:6444-6448; Poljak, R. J., et al. (1994) Structure 2:1121-1123). Still further, an antibody may be part of a larger immunoadhesion molecule, formed by covalent or noncovalent association of the antibody or antibody portion with one or more other proteins or peptides. Examples of such immunoadhesion molecules include use of the streptavidin core region to make a tetrameric scFv molecule (Kipriyanov, S. M., et al. (1995) Human Antibodies and Hybridomas 6:93-101) and use of a cysteine residue, a marker peptide and a C-terminal polyhistidine tag to make bivalent and biotinylated scFv molecules (Kipriyanov, S. M., et al. (1994) Mol. Immunol. 31:1047-1058).

[0049] Affinity Matured Antibody: “Affinity Matured Antibody” is used herein to refer to an antibody with one or more alterations in one or more CDRs, which result in an improvement in the affinity (i.e., KD, kd or ka) of the antibody for a target antigen compared to a parent antibody, which does not possess the alteration(s). Exemplary affinity matured antibodies will have nanomolar or even picomolar affinities for the target antigen. A variety of procedures for producing affinity matured antibodies are known in the art, including the screening of a combinatory antibody library that has been prepared using bio-display. For example, Marks et al., Biotechnology, 10: 779-783 (1992) describes affinity maturation by VH and VL domain shuffling. Random mutagenesis of CDR and / or framework residues is described by Barbas et al., Proc. Nat. Acad. Sci. USA, 91: 3809-3813 (1994); Schier et al., Gene, 169: 147-155 (1995); Yelton et al., J. Immunol., 155: 1994-2004 (1995); Jackson et al., J. Immunol., 154(7): 3310-3319 (1995); and Hawkins et al, J. Mol. Biol., 226: 889-896 (1992). Selective mutation at selective mutagenesis positions and at contact or hypermutation positions with an activity-enhancing amino acid residue is described in U.S. Pat. No. 6,914,128 B1.

[0050] Approximately: As used herein, the term “approximately” or “about,” as applied to one or more values of interest, refers to a value that is similar to a stated reference value. In certain embodiments, the term “approximately” or “about” refers to a range of values that fall within 15%, 14%, 13%, 12%, 11%, 10%, 9%, 8%, 7%, 6%, 5%, 4%, 3%, 2%, 1%, or less in either direction (greater than or less than) of the stated reference value unless otherwise stated or otherwise evident from the context (except where such number would exceed 100% of a possible value).

[0051] Baseline level: As used herein, the term “baseline level” refers to a value that represents the beginning level (including normal or diseased level) of a measurable quality, used for comparison with values representing response to an intervention (e.g., a drug, a medical procedural, or a control). In some embodiments, the baseline reflects the health state—disease severity, confounding conditions, biomarkers (e.g., hematological biomarkers) —present in a person or group of individuals at the beginning of a process. In some embodiments, the process is a medical treatment plan. In some embodiments, the process is a prospective study (e.g., clinical trial). In some embodiments, the baseline value is the last non-missing value before a subject starts the process (e.g., treatment plan or clinical trial). In some embodiments, the baseline value is the value before a subject suffers a condition (e.g., a condition associated with a myelodysplastic syndrome (MDS) described herein. In some embodiments, the subject experiences a change in values compared to the baseline value priorto receiving the drug, and treatment using the drug brings the values back to baseline levels. In some embodiments, treatment of a drug brings the values back to baseline levels more rapidly compared to a subject who did not receive the drug.

[0052] Comorbidity: As used herein, a “comorbidity” refers to one or more conditions or disorders that co-occur with (or are coincident with) a primary condition (such as a condition associated with MDS in an individual. In some embodiments, a subject having MDS is functionally iron deficient. In some embodiments, a functionally iron deficient subject with MDS has anemia. In some embodiments, a subject having MDS may have one or more of other comorbidities such as cardiac disease, CNS disease, pulmonary disease, hepatic disease, renal disease, malignancies, etc.

[0053] Control subject: A subject that has comparable features and property as the subject, e.g., age, species, state of health, and other similar parameters. In some embodiments, control subject may be a group of subjects having a similar condition (e.g., same gender, similar age, suffering from the same disease such as MDS) but is receiving, or is expected to receive a different treatment from the therapy described herein (e.g., treatment using an hemojuvelin antibody). In some embodiments, in an experiment or clinical trial, control subjects may be a group of participants who have characteristics similar to those of the treatment group, but they do not receive the treatment being studied. In some embodiments, the control subjects receive a substance or treatment which is designed to have no therapeutic value (i.e., a placebo).

[0054] CDR: As used herein, the term "CDR" refers to the complementarity determining region within antibody variable sequences. A typical antibody molecule comprises a heavy chain variable region (VH) and a light chain variable region (VL), which are usually involved in antigen binding. The VH and VL regions can be further subdivided into regions of hypervariability, also known as “complementarity determining regions” (“CDR”), interspersed with regions that are more conserved, which are known as “framework regions” (“FR”). Each VH and VL is typically composed of three CDRs and four FRs, arranged from amino-terminus to carboxy-terminus in the following order: FR1, CDR1, FR2, CDR2, FR3, CDR3, FR4. The extent of the framework region and CDRs can be precisely identified using methodology known in the art, for example, by the Kabat definition, the IMGT definition, the Chothia definition, the AbM definition, and / or the contact definition, all of which are well known in the art. See, e.g., Kabat, E.A., et al. (1991) Sequences of Proteins of Immunological Interest, Fifth Edition, U.S. Department of Health and Human Services, NIH Publication No. 91-3242; IMGT®, the international ImMunoGeneTics information system®http: / / www.imgt.org, Lefranc, M.-P. et al., Nucleic Acids Res., 27:209-212 (1999); Ruiz, M. et al., Nucleic Acids Res., 28:219-221 (2000); Lefranc, M.-P., Nucleic Acids Res., 29:207- 209 (2001); Lefranc, M.-P., Nucleic Acids Res., 31:307-310 (2003); Lefranc, M.-P. et al., In Silico Biol., 5, 0006 (2004) [Epub], 5:45-60 (2005); Lefranc, M.-P. et al., Nucleic Acids Res., 33:D593-597 (2005); Lefranc, M.-P. et al., Nucleic Acids Res., 37:D1006-1012 (2009); Lefranc, M.-P. et al., Nucleic Acids Res., 43:D413-422 (2015); Chothia et al., (1989) Nature 342:877; Chothia, C. et al. (1987) J. Mol. Biol. 196:901-917, Al-lazikani et al (1997) J. Molec. Biol. 273:927-948; and Almagro, J. Mol. Recognit. 17:132-143 (2004). ee also hgmp.mrc.ac.uk and bioinf.org.uk / abs. As used herein, a CDR may refer to the CDR defined by any method known in the art. Two antibodies having the same CDR means that the two antibodies have the same amino acid sequence of that CDR as determined by the same method, for example, the IMGT definition.

[0055] Generally, there are three CDRs in each of the variable regions of the heavy chain and the light chain, which are designated CDR1, CDR2 and CDR3, for each of the variable regions. The term "CDR set" as used herein refers to a group of three CDRs that occur in a single variable region capable of binding the antigen. The exact boundaries of these CDRs have been defined differently according to different systems. The system described by Kabat (Kabat et al., Sequences of Proteins of Immunological Interest (National Institutes of Health, Bethesda, Md. (1987) and (1991)) not only provides an unambiguous residue numbering system applicable to any variable region of an antibody, but also provides precise residue boundaries defining the three CDRs. These CDRs may be referred to as Kabat CDRs. Sub- portions of CDRs may be designated as L1, L2 and L3 or H1, H2 and H3 where the "L" and the "H" designates the light chain and the heavy chains regions, respectively. These regions may be referred to as Chothia CDRs, which have boundaries that overlap with Kabat CDRs. Other boundaries defining CDRs overlapping with the Kabat CDRs have been described by Padlan (FASEB J. 9:133-139 (1995)) and MacCallum (J Mol Biol 262(5):732-45 (1996)). Still other CDR boundary definitions may not strictly follow one of the above systems, but will nonetheless overlap with the Kabat CDRs, although they may be shortened or lengthened in light of prediction or experimental findings that particular residues or groups of residues or even entire CDRs do not significantly impact antigen binding. The methods used herein may utilize CDRs defined according to any of these systems, although exemplary embodiments use Kabat or Chothia defined CDRs.

[0056] CDR-grafted antibody: The term "CDR-grafted antibody" refers to antibodies which comprise heavy and light chain variable region sequences from one species but inwhich the sequences of one or more of the CDR regions of VH and / or VL are replaced with CDR sequences of another species, such as antibodies having murine heavy and light chain variable regions in which one or more of the murine CDRs (e.g., CDR3) has been replaced with human CDR sequences.

[0057] Chimeric antibody: The term "chimeric antibody" refers to antibodies which comprise heavy and light chain variable region sequences from one species and constant region sequences from another species, such as antibodies having murine heavy and light chain variable regions linked to human constant regions.

[0058] Complementary: As used herein, the term “complementary” refers to the capacity for precise pairing between two nucleotides or two sets of nucleotides. In particular, complementary is a term that characterizes an extent of hydrogen bond pairing that brings about binding between two nucleotides or two sets of nucleotides. For example, if a base at one position of an oligonucleotide is capable of hydrogen bonding with a base at the corresponding position of a target nucleic acid (e.g., an mRNA), then the bases are considered to be complementary to each other at that position. Base pairings may include both canonical Watson-Crick base pairing and non-Watson-Crick base pairing (e.g., Wobble base pairing and Hoogsteen base pairing). For example, in some embodiments, for complementary base pairings, adenosine-type bases (A) are complementary to thymidine- type bases (T) or uracil-type bases (U), that cytosine-type bases (C) are complementary to guanosine-type bases (G), and that universal bases such as 3-nitropyrrole or 5-nitroindole can hybridize to and are considered complementary to any A, C, U, or T. Inosine (I) has also been considered in the art to be a universal base and is considered complementary to any A, C, U or T.

[0059] Conservative amino acid substitution: As used herein, a “conservative amino acid substitution” refers to an amino acid substitution that does not alter the relative charge or size characteristics of the protein in which the amino acid substitution is made. Variants can be prepared according to methods for altering polypeptide sequence known to one of ordinary skill in the art such as are found in references which compile such methods, e.g. Molecular Cloning: A Laboratory Manual, J. Sambrook, et al., eds., Fourth Edition, Cold Spring Harbor Laboratory Press, Cold Spring Harbor, New York, 2012, or Current Protocols in Molecular Biology, F.M. Ausubel, et al., eds., John Wiley & Sons, Inc., New York. Conservative substitutions of amino acids include substitutions made amongst amino acids within the following groups: (a) M, I, L, V; (b) F, Y, W; (c) K, R, H; (d) A, G; (e) S, T; (f) Q, N; and (g) E, D.

[0060] Cross-reactive: As used herein and in the context of a targeting agent (e.g., antibody), the term “cross-reactive,” refers to a property of the agent being capable of specifically binding to more than one antigen of a similar type or class (e.g., antigens of multiple homologs, paralogs, or orthologs) with similar affinity or avidity. For example, in some embodiments, an antibody that is cross-reactive against human and non-human primate antigens of a similar type or class (e.g., a human hemojuvelin and non-human primate hemojuvelin) is capable of binding to the human antigen and non-human primate antigens with a similar affinity or avidity. In some embodiments, an antibody is cross-reactive against a human antigen and a rodent antigen of a similar type or class. In some embodiments, an antibody is cross-reactive against a rodent antigen and a non-human primate antigen of a similar type or class. In some embodiments, an antibody is cross-reactive against a human antigen, a non-human primate antigen, and a rodent antigen of a similar type or class.

[0061] Effective Amount: As used herein, “an effective amount” or “an amount effective” refers to the amount of each active agent (e.g., hemojuvelin antagonist including an anti-HJV antibody) required to confer therapeutic effect on the subject (such as in treating a condition associated with MDS, for example, anemia, either alone or in combination with one or more other active agents).

[0062] Erythropoiesis: As used herein, the term “erythropoiesis” refers to the process of producing red blood cells (RBCs or erythrocytes). In some embodiments, erythropoiesis comprises development from hematopoietic stem cells to mature red blood cells. For example, in the process of red blood maturation, a cell generally undergoes a series of differentiation steps, which may include, in the bone marrow, hemocytoblasts (a multipotent hematopoietic stem cells) differentiating along a path comprising one or more of common myeloid progenitors, unipotent stem cells, proerythroblasts, erythroblasts, polychromatophilic cells, and orthochromatic cells. In some embodiments, nuclear expulsion occurs at the end of the orthochromatic stage through an asymmetric division of the orthochromatic erythroblast, becoming a reticulocyte, which is an immature red blood cell. The reticulocytes are generally released from the bone marrow into the circulation, and ultimately become "erythrocytes" or mature red blood cells one or two days later. Therefore, reticulocytes are primarily present in circulating blood. In some embodiments, by the reticulocyte stage, the cell has extruded its nucleus, but is still capable of producing hemoglobin. In further embodiments, normal RBC count in a subject is in the range of 4.7x1012to 6.1x1012cells / L in men or 4.2x1012to 5.4x1012cells / L.

[0063] Ferritin: As used herein, the term “ferritin” refers to a protein that stores iron in cells, e.g., liver, spleen, and / or bone marrow, and releases it in a controlled fashion. It is the primary intracellular iron-storage protein in both prokaryotes and eukaryotes, keeping iron in a soluble and non-toxic form. In humans, it acts as a buffer against iron deficiency and iron overload. Circulating ferritin is also an indirect marker of the total amount of iron stored in the body; hence, serum ferritin is used as a diagnostic test for iron-deficiency anemia.

[0064] Framework: As used herein, the term "framework" or "framework sequence" refers to the remaining sequences of a variable region minus the CDRs. Because the exact definition of a CDR sequence can be determined by different systems, the meaning of a framework sequence is subject to correspondingly different interpretations. The six CDRs (CDR-L1, CDR-L2, and CDR-L3 of light chain and CDR-H1, CDR-H2, and CDR-H3 of heavy chain) also divide the framework regions on the light chain and the heavy chain into four sub- regions (FR1, FR2, FR3 and FR4) on each chain, in which CDR1 is positioned between FR1 and FR2, CDR2 between FR2 and FR3, and CDR3 between FR3 and FR4. Without specifying the particular sub-regions as FR1, FR2, FR3 or FR4, a framework region, as referred by others, represents the combined FRs within the variable region of a single, naturally occurring immunoglobulin chain. As used herein, a FR represents one of the four sub-regions, and FRs represents two or more of the four sub-regions constituting a framework region. Human heavy chain and light chain acceptor sequences are known in the art. In one embodiment, the acceptor sequences known in the art may be used in the antibodies disclosed herein.

[0065] Hemojuvelin (HJV): As used herein, the term “hemojuvelin (HJV)” (also known as repulsive guidance molecule C (RGMc) or hemochromatosis type 2 protein (HFE2)) refers to a membrane-bound and soluble form protein that regulates hepcidin production through the bone morphogenic protein (BMP) / SMAD signaling pathway (Xiao et al., “Bone morphogenic proteins in iron homeostasis.” Bone. 2020; 138:115495). The HFE2 gene encodes two known classes of glycosylphosphatidylinositol (GPI)-anchored and glycosylated HJV molecules, which are targeted to the membrane and undergo distinct fates. HJV exists in multiple isoforms, including two soluble isoforms and two membrane-associated isoforms. In some embodiments, a predominant membrane-associated isoform is a disulfide-linked two-chain form composed of N- and C-terminal fragments. In some embodiments, a full-length single- chain isoform associates with the membrane but is released from the cell surface and accumulates in extracellular fluid. In some embodiments, HJV may be of human (NCBI Gene ID 148738), non-human primate (e.g., NCBI Gene ID 698805), or rodent (e.g., NCBI GeneID 69585 or NCBI Gene ID 310681) origin. In addition to HJV (RGMc), the repulsive guidance molecule family includes repulsive guidance molecule A (RGMa) and repulsive guidance molecule B (RGMb). RGMa and RGMb are expressed in the central nervous system during development and are thought to be involved in controlling axonal patterning and neuronal survival, while HJV is produced in the liver and in cardiac and skeletal muscle.

[0066] Hepcidin: As used herein, a “hepcidin” refers to an iron-regulating peptide hormone primarily made in the liver that is encoded by the HAMP gene. In some embodiments, hepcidin controls the delivery of iron to blood plasma from intestinal cells absorbing iron, from erythrocyte-recycling macrophages, and from iron-storing hepatocytes. Normal hepcidin levels vary depending on the measurement technique, gender, tissue or fluid in which it is measured, and / or menopausal status. In some embodiments, hepcidin inhibits iron transport by binding to the iron export channel ferroportin which is located on the basolateral surface of gut enterocytes and the plasma membrane of reticuloendothelial cells (macrophages). In some embodiments, inhibiting ferroportin prevents iron from being exported and the iron is sequestered in the cells. In some embodiments, by inhibiting ferroportin, hepcidin prevents enterocytes from allowing iron into the hepatic portal system, thereby reducing dietary iron absorption. Hepcidin expression involves multiple aspects, including, for example, transcription of the HAMP gene, translation of the transcribed mRNA, and the posttranslational processing of the hepcidin precursor into the bioactive hepcidin-25 peptide (DTHFPICIFCCGCCHRSKCGMCCKT (SEQ ID NO: 129)). In some embodiments, hepcidin expression is modulated via the hemojuvelin-induced BMP signaling pathway. In some embodiments, hepcidin expression is modulated via the IL-6-JAK-STAT signaling pathway.

[0067] Hepcidin Antagonist: As used herein, a “hepcidin antagonist” refers to an agent that reduces hepcidin expression and / or hepcidin activity (directly or indirectly). In some embodiments, a hepcidin antagonist inhibits hepcidin-induced ferroportin degradation. Accordingly, in some embodiments, a hepcidin antagonist targets hepcidin function indirectly through the hepcidin stimulatory pathway to decrease hepcidin expression. In some embodiments, a hepcidin antagonist targets hepcidin function directly, e.g., by binding the hepcidin peptide to sequester free hepcidin or by binding ferroportin to inhibit the hepcidin- ferroportin binding interaction, thereby decreasing hepcidin-induced ferroportin degradation. In some embodiments, a hepcidin antagonist is a ferroportin inhibitor that disrupts ferroportin-hepcidin interactions, such as, for example, as disclosed in Ross SL, et al., Identification of Antibody and Small Molecule Antagonists of Ferroportin-HepcidinInteraction. Front Pharmacol. 2017 Nov 21;8:838; Fung E., et al., High-Throughput Screening of Small Molecules Identifies Hepcidin Antagonists. Molecular Pharmacology March 2013, 83 (3) 681-690; and Angeliki Katsarou and Kostas Pantopoulos, Hepcidin Therapeutics. Pharmaceuticals (Basel). 2018 Dec; 11(4): 127, the relevant contents of each of which are incorporated herein by reference.

[0068] Hemoglobin: As used herein, the term “hemoglobin (Hb)” refers to is the iron- containing oxygen-transport metalloprotein in red blood cells (erythrocytes). Hemoglobin in blood carries oxygen from the respiratory organs (e.g., lungs or gills) to the rest of the body (i.e., tissues). There it releases the oxygen to permit aerobic respiration to provide energy to power functions of an organism in the process called metabolism. A healthy individual human has about 12 to 20 g / dL of hemoglobin in blood. Hemoglobin (Hb) is synthesized in a complex series of steps. The heme part is synthesized in a series of steps in the mitochondria and the cytosol of immature red blood cells, while the globin protein parts are synthesized by ribosomes in the cytosol. Iron is an essential element for hemoglobin synthesis, particularly heme synthesis. The final step of heme synthesis is the addition of an iron ion to protoporphyrin IX, a precursor of heme, by ferrochelatase, thereby producing a heme molecule. Globin chain production occurs in the cytosol of erythrocytes and occurs by genetic transcription and translation. In some embodiments, the presence of heme induces globin production. Heme combines with globin to form hemoglobin.

[0069] Human antibody: The term "human antibody", as used herein, is intended to include antibodies having variable and constant regions derived from human germline immunoglobulin sequences. The human antibodies of the disclosure may include amino acid residues not encoded by human germline immunoglobulin sequences (e.g., mutations introduced by random or site-specific mutagenesis in vitro or by somatic mutation in vivo), for example in the CDRs and in particular CDR3. However, the term "human antibody", as used herein, is not intended to include antibodies in which CDR sequences derived from the germline of another mammalian species, such as a mouse, have been grafted onto human framework sequences (e.g., CDRs grafted in a heterologous framework).

[0070] Humanized antibody: The term "humanized antibody" refers to antibodies which comprise heavy and light chain variable region sequences from a non-human species (e.g., a mouse) but in which at least a portion of the VHand / or VLsequence has been altered to be more "human-like", i.e., more similar to human germline variable sequences. One type of humanized antibody is a CDR-grafted antibody, in which human CDR sequences are introduced into non-human VHand VLsequences to replace the corresponding nonhumanCDR sequences. In one embodiment, humanized anti-hemojuvelin antibodies and antigen binding portions are provided. Such antibodies may be generated by obtaining murine anti- hemojuvelin monoclonal antibodies using traditional hybridoma technology followed by humanization using in vitro genetic engineering, such as those disclosed in Kasaian et al PCT publication No. WO 2005 / 123126 A2.

[0071] Isolated antibody: An "isolated antibody", as used herein, is intended to refer to an antibody that is substantially free of other antibodies having different antigenic specificities (e.g., an isolated antibody that specifically binds hemojuvelin is substantially free of antibodies that specifically bind antigens other than hemojuvelin). An isolated antibody that specifically binds hemojuvelin may, however, have cross-reactivity to other antigens, such as other repulsive guidance molecule (RGM) proteins (e.g., RGMa and / or RGMb). Moreover, an isolated antibody may be substantially free of other cellular material and / or chemicals.

[0072] Kabat numbering: The terms "Kabat numbering", "Kabat definitions and "Kabat labeling" are used interchangeably herein. These terms, which are recognized in the art, refer to a system of numbering amino acid residues which are more variable (i.e. hypervariable) than other amino acid residues in the heavy and light chain variable regions of an antibody, or an antigen binding portion thereof (Kabat et al. (1971) Ann. NY Acad, Sci. 190:382-391 and, Kabat, E. A., et al. (1991) Sequences of Proteins of Immunological Interest, Fifth Edition, U.S. Department of Health and Human Services, NIH Publication No. 91-3242). For the heavy chain variable region, the hypervariable region ranges from amino acid positions 31 to 35 for CDR1, amino acid positions 50 to 65 for CDR2, and amino acid positions 95 to 102 for CDR3. For the light chain variable region, the hypervariable region ranges from amino acid positions 24 to 34 for CDR1, amino acid positions 50 to 56 for CDR2, and amino acid positions 89 to 97 for CDR3.

[0073] Mean corpuscular hemoglobin (MCH): As used herein, the term “mean corpuscular hemoglobin” refers to the average mass of hemoglobin (Hgb) per red blood cell (RBC) in a sample of blood. It is calculated by dividing the total mass of hemoglobin by the number of red blood cells in a volume of blood: MCH=(Hgb*10) / RBC.

[0074] In some embodiments, a normal MCH value in humans is 27 to 31 picograms (pg) / cell. The amount of hemoglobin per RBC depends on hemoglobin synthesis and the size of the RBC. The mass of the red cell is determined by the iron (as part of the hemoglobin molecule), thus MCH in picograms is roughly the mass of one red cell. In some embodiments, in iron deficiency anemia the cell mass becomes lighter, and a MCH below 27 pg is an indication of iron deficiency.

[0075] Mean corpuscular hemoglobin concentration (MCHC): As used herein, the term “mean corpuscular hemoglobin concentration” refers to the amount of hemoglobin per unit volume. MCHC correlates the hemoglobin content with the volume of the cell. MCHC is expressed as g / dl of red blood cells or as a percentage value. In some embodiments, a normal value for MCHC in humans is 34 ± 2 g / dl.

[0076] Recombinant antibody: The term "recombinant human antibody", as used herein, is intended to include all human antibodies that are prepared, expressed, created or isolated by recombinant means, such as antibodies expressed using a recombinant expression vector transfected into a host cell (described in more details in this disclosure), antibodies isolated from a recombinant, combinatorial human antibody library (Hoogenboom H. R., (1997) TIB Tech. 15:62-70; Azzazy H., and Highsmith W. E., (2002) Clin. Biochem. 35:425-445; Gavilondo J. V., and Larrick J. W. (2002) BioTechniques 29:128-145; Hoogenboom H., and Chames P. (2000) Immunology Today 21:371-378), antibodies isolated from an animal (e.g., a mouse) that is transgenic for human immunoglobulin genes (see e.g., Taylor, L. D., et al. (1992) Nucl. Acids Res. 20:6287-6295; Kellermann S-A., and Green L. L. (2002) Current Opinion in Biotechnology 13:593-597; Little M. et al (2000) Immunology Today 21:364-370) or antibodies prepared, expressed, created or isolated by any other means that involves splicing of human immunoglobulin gene sequences to other DNA sequences. Such recombinant human antibodies have variable and constant regions derived from human germline immunoglobulin sequences. In certain embodiments, however, such recombinant human antibodies are subjected to in vitro mutagenesis (or, when an animal transgenic for human Ig sequences is used, in vivo somatic mutagenesis) and thus the amino acid sequences of the VH and VL regions of the recombinant antibodies are sequences that, while derived from and related to human germline VHand VLsequences, may not naturally exist within the human antibody germline repertoire in vivo. One embodiment of the disclosure provides fully human antibodies capable of binding human hemojuvelin which can be generated using techniques well known in the art, such as, but not limited to, using human Ig phage libraries such as those disclosed in Jermutus et al., PCT publication No. WO 2005 / 007699 A2.

[0077] Selective: As used herein, the term “selective” or “selectively” refers to the ability of a molecule to produce an effect in relation to its target molecule compared to a reference molecule. For example, a molecule that selectively inhibits its target molecule means that this molecule is capable of inhibiting its target molecule with a degree that is distinguishable from a reference molecule in an inhibition assay or other inhibitory context. For example, with respect to an inhibitor, the term, “selectively inhibits”, refers to the ability of the inhibitor toinhibit its target molecule with a degree that is distinguishable from a reference molecule that is not substantially inhibited in an inhibition assay, e.g., to an extent that permit selective inhibition of the target molecule, as described herein. For example, the half maximal inhibitory concentration (IC50) for the target molecule and / or the reference molecule can be tested in a kinase potency assay as described in Asshoff, M. et al., Momelotinib inhibits ACVR1 / ALK2, decreases hepcidin production, and ameliorates anemia of chronic disease in rodents. Blood. 2017 Mar 30; 129(13): 1823-1830 (e.g., Kinase potency assay by Carna Biosciences). In this assay, inhibitor solution (e.g., solution containing the selective inhibitor to be tested) / kinase substrate is mixed with target molecule solution (e.g., ALK2) or reference molecule solution (e.g., JAK1 or JAK2), and incubated under room temperature for 1 hour. Once the reaction is terminated, the signal produced by enzymatic activity on the substrate can be measured. The half maximal inhibitor concentration for the target molecule and the reference molecule can be calculated. In some embodiments, a molecule described herein selectively binds to a target molecule. In some embodiments, a molecule described herein selectively inhibits to a target molecule. In some embodiments, a molecule described herein selectively antagonizes to a target molecule. In some embodiments, a molecule described herein selectively neutralizes to a target molecule.

[0078] Specifically binds: As used herein, the term “specifically binds” refers to the ability of a molecule to bind to a binding partner with a degree of affinity or avidity that enables the molecule to be used to distinguish the binding partner from an appropriate control in a binding assay or other binding context. With respect to an antibody, the term, “specifically binds”, refers to the ability of the antibody to bind to a specific antigen with a degree of affinity or avidity, compared with an appropriate reference antigen or antigens, that enables the antibody to be used to distinguish the specific antigen from others, e.g., to an extent that permits preferential targeting to certain cells, e.g., muscle cells, through binding to the antigen, as described herein. In some embodiments, an antibody specifically binds to a target if the antibody has a KDfor binding the target of at least about 10-4M, 10-5M, 10-6M, 10-7M, 10-8M, 10-9M, 10-10M, 10-11M, 10-12M, 10-13M, or less. In some embodiments, an antibody specifically binds to hemojuvelin.

[0079] Subject: As used herein, the term “subject” refers to a mammal. In some embodiments, a subject is non-human primate, or rodent. In some embodiments, a subject is a human. In some embodiments, a subject is a patient, e.g., a human patient that has or is suspected of having a disease. In some embodiments, the subject is a human patient who has or is suspected of having a condition associated with MDS. In some embodiments, the subjectis a human patient having MDS and is suspected of having a condition associated with functional iron deficiency.

[0080] Transferrin Saturation (TSAT%): As used herein, the term “transferrin saturation (TSAT%),” refers to a percentage value of serum iron divided by the total iron-binding capacity of the available transferrin, the main protein that binds iron in the blood. This value indicates how much serum iron is bound to transferrin. For instance, a value of 15% means that 15% of iron-binding sites of transferrin are being occupied by iron. A low transferrin saturation is a common indicator of iron deficiency whereas a high transferrin saturation may indicate iron overload or hemochromatosis. Transferrin saturation is also called transferrin saturation index (TSI) or transferrin saturation percentage (TS%).

[0081] Treatment: As used herein, the term “treating” or “treatment” refers to the application or administration of a composition including one or more active agents to a subject, who has a target disease or disorder, a symptom of the disease / disorder, or a predisposition toward the disease / disorder, with the purpose to cure, heal, alleviate, relieve, alter, remedy, ameliorate, improve, or affect the disorder, the symptom of the disease, or the predisposition toward the disease or disorder. Alleviating a target disease / disorder includes delaying or preventing the development or progression of the disease, or reducing disease severity. II. Methods for Treating MDS

[0082] According to some aspects, the disclosure provides compositions and methods for treating a subject having MDS, the method comprising administering to the subject a hemojuvelin (HJV) antagonist (e.g., anti-HJV antibody). In some aspects, the disclosure provides a method of treating myelodysplastic syndrome (MDS) comprising administering an anti-HJV antibody to a functionally iron deficient subject having MDS. In some aspects, the disclosure provides a method of treating myelodysplastic syndrome (MDS) comprising administering an anti-HJV antibody to a subject having MDS, wherein the subject has elevated hepcidin levels. In some embodiments, the subject with MDS is functionally iron deficient, and the administration results in release of cellular iron stores. In some embodiments, administration of an anti-HJV antibody results in release of cellular iron stores in the amount sufficient to treat anemia in the subject (e.g., a functionally iron deficient subject having MDS). In some embodiments, administration of an anti-HJV antibody decreases hepcidin levels in the subject.

[0083] Myelodysplastic syndrome (MDS), also known as myelodysplastic neoplasm, refers to a heterogenous family of clonal hematopoietic disorders. In some embodiments, MDS is characterized by ineffective hematopoiesis, morphologic dysplasia in hematopoietic cells, bone marrow failure, and refractory cytopenia in the peripheral blood (e.g., Hb <10g / dL; platelets <100x109 / L; and / or absolute neutrophil count <1.8x109 / L). In addition, several cytogenic manifestations associated with MDS are also described herein.

[0084] In early stages, an MDS may be asymptomatic. As an MDS progresses, symptoms increase in occurrence and severity, with common symptoms including, for example, cytopenia including refractory anemia, thrombocytopenia, and neutropenia. In late stages, common symptoms of MDSs include, but are not limited to, hematopoietic insufficiency, increased susceptibility to infection, and signs of bleeding. MDSs of increased severity (e.g., high MDS) may also evolve into acute myeloid leukemia (AML). In some embodiments, MDS is primary MDS. Primary MDS, also known as de novo MDS or “primitive” MDS (p-MDS), is any MDS for which the cause of MDS is unidentified. In some embodiments, MDS is secondary MDS. Secondary MDS, also known as therapy-related MDS (t-MDS), is an MDS for which there is a suspected cause; typically, MDS is classified as secondary MDS when a subject having or at risk of developing MDS had a previous non- myeloid neoplasm, for which the subject received chemotherapy and / or radiotherapy. Exemplary differences between primary MDS and secondary MDS are described in Leone, G., et al. (2022). Mediterranean Journal of Hematology and Infectious Diseases, 14(1):e2022030.

[0085] Several MDS conditions are known; however, art-established categories of MDS have been revised by the World Health Organization (WHO) several times, including in 2016 (see: Arber, D. A., et al. (2016). Blood, The Journal of the American Society of Hematology, 127(20), 2391-2405) and in 2022 (see: Khoury, J. D., et al. (2022). Leukemia, 36(7), 1703-1719.). Though revisions to the classification of MDS in 2016 primarily refined the cytopenia and morphological changes described in previous classifications, the most recent revision of 2022 provided new, non-synonymous classifications of MDSs based on several factors. A detailed analysis of these changes is provided in Zhang, Y., et al., (2022). Leukemia, 36(12), 2875-2882. References made herein to particular MDS conditions can be understood to reference the 2016 WHO classification of MDS, which includes 6 main categories: MDS with single lineage dysplasia (MDS-SLD), MDS with ring sideroblasts (MDS-RS), MDS with multilineage dysplasia (MDS-MLD), MDS with excess blasts (MDS- EB), MDS with isolated del(5q), and MDS, unclassifiable (MDS-U). Those of skill in the artwill understand that the peripheral blood biomarkers, bone marrow biomarkers, and cytogenic profiles described herein for each MDS condition may be helpful for identifying the corresponding 2022 WHO classification (e.g., as per Zhang et al., (2022)).

[0086] In some embodiments, a subject having or at risk of developing MDS has dysplasia of one or more myeloid lineages (e.g., erythroid, granulocytic, or megakaryocytic). Dysplasia, as used herein, refers to an abnormal growth or development of cells within tissue (e.g., bone marrow), wherein the cells are not necessarily cancerous. Dysplasia of myeloid lineages can be identified by abnormal size and / or number of immature cells in the bone marrow. In some embodiments, the dysplasia is erythroid dysplasia. In some embodiments, the dysplasia is granulocytic dysplasia. In some embodiments, the dysplasia is megakaryocytic dysplasia. In some embodiments, a subject having or at risk of developing MDS has dysplasia of two or more myeloid lineages. In some embodiments, a subject having or at risk of developing MDS has dysplasia of two myeloid lineages. In some embodiments, a subject having or at risk of developing MDS has erythroid dysplasia and granulocytic dysplasia. In some embodiments, a subject having or at risk of developing MDS has erythroid dysplasia and megakaryocytic dysplasia. In some embodiments, a subject having or at risk of developing MDS has granulocytic dysplasia and megakaryocytic dysplasia. In some embodiments, a subject having or at risk of developing MDS has dysplasia of three or more myeloid lineages. In some embodiments, a subject having or at risk of developing MDS has erythroid dysplasia, granulocytic dysplasia, and megakaryocytic dysplasia.

[0087] In some embodiments, a subject having or at risk of developing MDS has presence of blasts in the peripheral blood. Blasts, also referred to as myeloblasts, are immature cells of the granulocytic lineage, and reside in the bone marrow. Blasts are not normally present in the peripheral blood; their presence indicates failure or deficiencies of hemopoiesis, as seen, for example, in certain types of anemia. In some embodiments, a subject having or at risk of developing MDS does not have blasts present in the peripheral blood.

[0088] In some embodiments, a subject having or at risk of developing MDS has or is at risk of developing MDS with single lineage dysplasia. MDS with single lineage dysplasia (MDS-SLD; formerly known as “refractory cytopenia with unilineage dysplasia”), refers to an MDS characterized by a single dysplastic lineage, one or two refractory cytopenias, low presence or absence of ring sideroblasts in the bone marrow (<15%), and low presence or absence of blasts in peripheral blood (<1%) or in the bone marrow (<5%). In some embodiments, a subject having MDS-SLD does not have ring sideroblasts in the bonemarrow. In some embodiments, the refractory cytopenia in MDS-SLD includes refractory anemia, refractory neutropenia, and / or refractory thrombocytopenia. In some embodiments, abnormal karyotypes may be observed in patients with MDS-SLD. In some embodiments, a subject having MDS-SLD does not have isolated del(5q). In some embodiments, one or more somatic mutations may occur in MDS-SLD but MDS-SLD is not associated with any particular somatic mutation. In some embodiments, a subject has or is at risk of developing MDS-SLD. In some embodiments, a subject has or is at risk of developing primary MDS- SLD. In some embodiments, a subject has or is at risk of developing secondary MDS-SLD. In some embodiments, a subject does not have secondary MDS-SLD.

[0089] In some embodiments, a subject having or at risk of developing MDS has or is at risk of developing MDS with multilineage dysplasia. MDS with multilineage dysplasia (MDS-MLD; formerly known as refractory cytopenias with multilineage dysplasia), refers to an MDS characterized by multiple dysplastic lineages, one or more refractory cytopenias, low presence or absence of ring sideroblasts in the bone marrow (<15%), and low presence or absence of blasts in peripheral blood (<1%) or in the bone marrow (<5%). In some embodiments, a subject having MDS-MLD does not have ring sideroblasts in the bone marrow. In some embodiments, the refractory cytopenia in MDS-MLD includes refractory anemia, refractory neutropenia, and / or refractory thrombocytopenia. In some embodiments, abnormal karyotypes may be observed in patients with MDS-MLD. In some embodiments, a subject having MDS-MLD does not have isolated del(5q). In some embodiments, one or more somatic mutations may occur in MDS-MLD but MDS-MLD is not associated with any particular somatic mutation. In some embodiments, a subject has or is at risk of developing MDS-MLD. In some embodiments, a subject has or is at risk of developing primary MDS- MLD. In some embodiments, a subject has or is at risk of developing secondary MDS-MLD. In some embodiments, a subject does not have secondary MDS-MLD.

[0090] In some embodiments, a subject having or at risk of developing MDS has or is at risk of developing MDS with ringed sideroblasts. MDS with ringed sideroblasts (MDS-RS; formerly known as refractory anemia with ringed sideroblasts”), refers to an MDS characterized by presence of ring sideroblasts in the bone marrow (≥15%), one or two refractory cytopenias, low presence of and low presence or absence of blasts in peripheral blood (<1%) or in the bone marrow (<5%). In some embodiments, a subject having or at risk of developing MDS has ring sideroblasts. As used herein, the term “ring sideroblasts” (RS) refers to nucleated erythrocytes in the bone marrow, wherein the erythrocytes have granules of iron accumulated in the mitochondria surrounding the nucleus of the cell, such that a ringof five or more iron granules encircles a third or more of the nucleus. Ring sideroblasts can be detected by, for example, analysis of bone marrow aspirate smears. In some embodiments, ring sideroblasts are associated with functional iron deficiency, wherein iron accumulates in the erythrocytes but cannot be incorporated into hemoglobin. In some embodiments, ring sideroblasts are associated with anemia (e.g., sideroblastic anemia). MDS-RS may manifest with single lineage dysplasia (MDS-RS-SLD) or multilineage dysplasia (MDS-RS-MLD). In some embodiments, the refractory cytopenia in MDS-RA includes refractory anemia, refractory neutropenia, and / or refractory thrombocytopenia. In some embodiments, a subject having MDS-RS shows abnormal karyotypes. In some embodiments, a subject having MDS- RA does not have isolated del(5q). In some embodiments, MDS-RS is associated with SF3B1 mutation. In some embodiments, a subject has or is at risk of developing MDS-RS. In some embodiments, a subject has or is at risk of developing MDS-RS-SLD. In some embodiments, a subject has or is at risk of developing MDS-RS-MLD. In some embodiments, a subject has or is at risk of developing primary MDS-RS. In some embodiments, a subject does not have MDS-RS. In some embodiments, a subject does not have MDS-RS-SLD. In some embodiments, a subject does not have MDS-RS-MLD. In some embodiments, a subject does not have primary MDS-RS. In some embodiments, a subject has or is at risk of developing secondary MDS-RS. In some embodiments, a subject does not have secondary MDS-RS.

[0091] In some embodiments, a subject having or at risk of developing MDS has or is at risk of developing MDS with excess blasts (MDS-EB). MDS with excess blasts (MDS-EB; formerly known as refractory anemia with excess blasts), refers to an MDS characterized by excess blasts in the peripheral blood (≥2%) and bone marrow (≥5%), one or more refractory cytopenias. MDS-EB is divided into MDS-EB-1 and MDS-EB-2, depending on the number of excess blasts in the peripheral blood and bone marrow. In MDS-EB-1, excess blasts range between about 2-4% in the peripheral blood and about 5-9% in the bone marrow. In MDS- EB-2, excess blasts range between about 5-19% in the peripheral blood and about 10-19% the bone marrow; in some instances, MDS-EB-2 manifests with the presence of Auer rods. Auer rods are large crystalline cytoplasmic inclusion bodies composed of fused lysosomes. Auer rods are specifically found in certain myeloid neoplasms. Auer rods can be detected by, for example, analysis of bone marrow aspirate smears. In some embodiments, a subject having or at risk of developing MDS do not have presence of Auer rods in blasts. In some embodiments, MDS-EB manifests with no dysplastic lineages. In some embodiments, MDS- EB manifests with single lineage dysplasia or multilineage dysplasia. In some embodiments, the refractory cytopenia in MDS-EB includes refractory anemia, refractory neutropenia,and / or refractory thrombocytopenia. In some embodiments, abnormal karyotypes may be observed in patients with MDS-EB. In some embodiments, MDS-EB is associated with mutations in FLT3. In some embodiments, MDS-EB can occur with one or more different somatic mutations other than FLT3. In some embodiments, a subject has or is at risk of developing MDS-EB. In some embodiments, a subject has or is at risk of developing MDS- EB-1. In some embodiments, a subject has or is at risk of developing MDS-EB-2. In some embodiments, a subject has or is at risk of developing primary MDS-EB. In some embodiments, a subject has or is at risk of developing secondary MDS-EB.

[0092] In some embodiments, a subject having or at risk of developing MDS has or is at risk of developing MDS with isolated del(5q). As used herein, the term “MDS with isolated del(5q)” (MDS-del(5q)) refers to an MDS characterized by a cytogenic abnormality comprising an isolated deletion between bands q21 and q32 on the long arm of chromosome 5 (del(5q)) and excluding a deletion of 7q (del(7q)) or a chromosome 7 monosomy (-7). MDS-del(5q) is typically characterized by one or more dysplastic lineage, one or two refractory cytopenias, and low presence or absence of blasts in peripheral blood (<1%) or in the bone marrow (<5%). MDS-del(5q) typically manifests with absence of Auer rods and absence of ring sideroblasts. In some embodiments, MDS-del(5q) manifests with single lineage dysplasia or multilineage dysplasia. In some embodiments, the refractory cytopenia in MDS-del(5q) includes refractory anemia, refractory neutropenia, and / or refractory thrombocytopenia. In some embodiments, one or more somatic mutations may occur in MDS-del(5q). In some embodiments, MDS-del(5q) is not associated with any particular somatic mutation. In some embodiments, a subject has or is at risk of developing MDS- del(5q). In some embodiments, a subject has or is at risk of developing primary MDS- del(5q). In some embodiments, a subject has or is at risk of developing secondary MDS- del(5q).

[0093] In some embodiments, a subject having or at risk of developing MDS has or is at risk of developing MDS, unclassified. MDS, unclassified (MDS-U) refers to an overlapping MDS / MPN category characterized features of proliferation which are found in MPN, but also the types of dysplasia found in MDS. MDS-U encompasses less than 5% of myeloid disorders. MDS-U is divided into MDS-U-BL, MDS-U-Pan, and MDS-U-CG. MDS-U-BL manifests with a refractory cytopenia with a unilineage or multilineage dysplasia, and 1% blasts in the peripheral blood. MDS-U-Pan manifests with pancytopenia with unilineage dysplasia. MDS-U-CG manifests with refractory cytopenia with less than <10% dysplastic cells, <5% blasts in the bone marrow, and presence of an MDS-relatedcytogenic abnormality. Though MDS-U is rare, and prediction of prognosis is difficult, in some cases, MDS-U-Pan and MDS-U-CG have a lower risk for evolution into AML (Margolskee, E., et al. (2017) American journal of clinical pathology vol. 148,1 (2017): 49- 57.). In some embodiments, MDS-U manifests with single lineage dysplasia or multilineage dysplasia. In some embodiments, the refractory cytopenia in MDS-U includes refractory anemia, refractory neutropenia, and / or refractory thrombocytopenia. In some embodiments, one or more somatic mutations can occur in MDS-U. In some embodiments, MDS-U is not strongly associated with any particular somatic mutation.

[0094] In some embodiments, a subject having or at risk of developing MDS has or is at risk of developing an MDS / myeloproliferative neoplasm (MDS / MPN) overlap syndrome. Myeloproliferative neoplasms (MPN) are a family of hematopoietic stem cell disorders associated with several mutations. MPNs include polycythemia vera, essential thrombocytosis, and primary myelofibrosis. MDS / MPN overlap syndromes are chronic clonal myeloid malignancies in which features of MDS and MPN are simultaneously present. MDS / MPN overlap syndromes include atypical chronic myeloid leukemia (aCML), chronic myelomonocytic leukemia (CMML), juvenile myelomonocytic leukemia (JMML), MDS / MPN with ring sideroblasts and thrombocytosis (MDS / MPN-RS-T), and MDS / MPN- unclassified (MDS / MPN-U). In some embodiments, a subject having or at risk of developing an MDS / MPN overlap syndrome has an abnormal karyotype. In some embodiments, a subject having or at risk of developing an MDS / MPN overlap syndrome has an aneuploidy. Several aneuploidies have been identified in MDS / MPN conditions, including, for example, trisomy 8 (+8), trisomy 9 (+9), monosomy 7 (-7). In some embodiments, a subject having or at risk of developing an MDS / MPN overlap syndrome has a deletion in one or more chromosomes. Several chromosomal deletions are associated with MDS / MPN overlap syndromes, for example, del(7q), del(13q), and del(20q). In some embodiments, a subject having or at risk of developing an MDS / MPN overlap syndrome has one or more somatic mutations. Though precise incidence of somatic mutations in MDS / MPN overlap syndromes is not yet estimated, mutations in RAS, JAK2, MPL, CBL, KIT, TET2, FLT3, CSF3R, SETBP1, NRAS, RUNX1, DNMT3A, ASXL1, MML, and EZH2 are associated with MDS / MPN overlap syndromes, as well as other myeloid neoplasms. MDS / MPN are described, e.g., in Fontana et al., Myelodysplastic Syndromes / Myeloproliferative Overlap Neoplasms and Differential Diagnosis in the WHO and ICC 2022 Era: A Focused Review, (2023), Cancers (Basel). 2023 Jun 13;15(12):3175, the entire contents of which are incorporated herein by reference.

[0095] In some embodiments, an MDS / MPN overlap syndrome is atypical chronic myeloid leukemia (aCML), e.g., according to ICC 2022 classification. aCML is classified as MDS / MPN with neutrophilia in WHO 2022 classification. In some embodiments, a subject having or at risk of developing MDS has or is at risk of developing aCML. Atypical chronic myeloid leukemia (aCML) is a BCR-ABL1 negative MDS / MPN overlap syndrome with a high rate of evolution to AML (about 40% of patients). aCML is characterized by splenomegaly, neutrophilic leukocytosis with left shift, and prominent granulocytic dysplasia. Neutrophil counts are typically high (>13x109 / L), with >10% leukocyte presence and <20% blasts in the peripheral blood and bone marrow. Other diagnostic criteria include: circulating immature a myeloid cells constituting ≥ 10% of WBC, with neutrophilic dysplasia, <10% monocytes, hypercellular with granulocytic hyperplasia and granulocytic dysplasia, with or without involvement of other lineages, and BCR::ABL1 or tyrosine kinase fusions associated with myeloid / lymphoid neoplasms with eosinophilia. Several somatic mutations are associated with aCML, for example: SETBP1, ASXL1, NRAS, KRAS, SRSF2, TET2, CBL, CSFR3, JAK2, EZH2, MPL, CSF3R, and ETNK1. For a review of aCML diagnosis and treatment, see: Crisa et al. (2020). International Journal of Molecular Science. 21(18), 6862. In some embodiments, a subject having MDS / MPN does not have mutations in JAK2, CALR, and / or MPL genes. In some embodiments, a subject having MDS / MPN with neutrophilia has recurrent mutations in ETNK1 and SETBP1 genes. In some embodiments, a subject having MDS / MPN with neutrophilia has recurrent mutations in ETNK1, SETBP1, and ASXL1 genes.

[0096] MDS / MPN with neutrophilia is a disorder that presents clinical features such as splenomegaly and neutrophilic leukocytosis. In some embodiments, MDS / MPN with neutrophilia predominantly affects the neutrophilic lineage associated with neutrophilic leukocytosis. In some embodiments, a subject having MDS / MPN with neutrophilia has circulating immature granulocytic precursors constituting at least 10% (e.g., at least 10%, at least 12%, at least 15%, at least 18%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, or more) of all leukocytes. In some embodiments, a subject having MDS / MPN with neutrophilia has circulating immature granulocytic precursors constituting 10%-95% (e.g., 10%-95%, 10%-90%, 10%-85%, 10%- 80%, 10%-75%, 10%-70%, 10%-65%, 10%-60%, 10%-55%, 10%-50%, 10%-45%, 10%- 40%, 10%-35%, 10%-30%, 10%-25%, 10%-20%, 10%-15%, 15%-95%, 15%-90%, 15%- 85%, 15%-80%, 15%-75%, 15%-70%, 15%-65%, 15%-60%, 15%-55%, 15%-50%, 15%-45%, 15%-40%, 15%-35%, 15%-30%, 15%-25%, 15%-20%, 20%-95%, 20%-90%, 20%- 85%, 20%-80%, 20%-75%, 20%-70%, 20%-65%, 20%-60%, 20%-55%, 20%-50%, 20%- 45%, 20%-40%, 20%-35%, 20%-30%, 20%-25%, 25%-95%, 25%-90%, 25%-85%, 25%- 80%, 25%-75%, 25%-70%, 25%-65%, 25%-60%, 25%-55%, 25%-50%, 25%-45%, 25%- 40%, 25%-35%, 25%-30%, 30%-95%, 30%-90%, 30%-85%, 30%-80%, 30%-75%, 30%- 70%, 30%-65%, 30%-60%, 30%-55%, 30%-50%, 30%-45%, 30%-40%, 30%-35%, 35%- 95%, 35%-90%, 35%-85%, 35%-80%, 35%-75%, 35%-70%, 35%-65%, 35%-60%, 35%- 55%, 35%-50%, 35%-45%, 35%-40%, 40%-95%, 40%-90%, 40%-85%, 40%-80%, 40%- 75%, 40%-70%, 40%-65%, 40%-60%, 40%-55%, 40%-50%, 40%-45%, 45%-95%, 45%- 90%, 45%-85%, 45%-80%, 45%-75%, 45%-70%, 45%-65%, 45%-60%, 45%-55%, 45%- 50%, 50%-95%, 50%-90%, 50%-85%, 50%-80%, 50%-75%, 50%-70%, 50%-65%, 50%- 60%, 50%-55%, 55%-95%, 55%-90%, 55%-85%, 55%-80%, 55%-75%, 55%-70%, 55%- 65%, 55%-60%, 60%-95%, 60%-90%, 60%-85%, 60%-80%, 60%-75%, 60%-70%, 60%- 65%, 65%-95%, 65%-90%, 65%-85%, 65%-80%, 65%-75%, 65%-70%, 70%-95%, 70%- 90%, 70%-85%, 70%-80%, 70%-75%, 75%-95%, 75%-90%, 75%-85%, 75%-80%, 80%- 95%, 80%-90%, 80%-85%, 85%-95%, 85%-90%, or 90%-95%) of all leukocytes. In some embodiments, MDS / MPN with neutrophilia also shows prominent granulocytic dysplasia (e.g., hypogranular and hypolobated neutrophils, abnormal chromatin clumping, and / or pseudo Pelger–Huet neutrophils). In some embodiments, a main differential diagnosis of MDS / MPN with neutrophilia is BCR::ABL1-positive CML. The presence of BCR::ABL1 translocation, can be detected by karyotype analysis, completed with molecular testing, such as reverse transcription polymerase chain reaction (RT-PCR) and fluorescence in situ hybridization (FISH) techniques. In some embodiments, a subject with MDS / MPN with neutrophilia is not suitable for treatment with tyrosine kinase inhibitors (e.g., imatinib or second- or third-generation Abelson inhibitors) due to the lack of BCR::ABL1 translocation.

[0097] In some embodiments, a subject having MDS / MPN with neutrophilia has a percentage of monocytes less than 10% (e.g., less than 10%, less than 9%, less than 8%, less than 7%, less than 6%, less than 5%, less than 4%, less than 3%, less than 2%, less than 1%, or less) of the total leukocytes.

[0098] In some embodiments, a subject having MDS / MPN with neutrophilia has a percentage of eosinophils less than 10% (e.g., less than 10%, less than 9%, less than 8%, less than 7%, less than 6%, less than 5%, less than 4%, less than 3%, less than 2%, less than 1%, or less) of the total leukocytes.

[0099] In some embodiments, a subject with MDS / MPN with neutrophilia having anemia is associated with worse prognosis (see, e.g., Klein et al., Characteristics, primary treatment, and survival of MDS / MPN with neutrophilia: a population-based study, Blood Adv. 2023 Nov 10;7(24):7554–7563). In some embodiments, an anti-HJV antibody described in herein improves anemia in a subject having MDS / MPN with neutrophilia. In some embodiments, an anti-HJV antibody described herein improves prognosis in a subject having MDS / MPN with neutrophilia. [000100] In some embodiments, an MDS / MPN overlap syndrome is MDS / MPN with ring sideroblasts and thrombocytosis. In some embodiments, a subject having or at risk of developing MDS has or is at risk of developing MDS / MPN-RS-T. In some embodiments, a subject does not have MDS / MPN-RS-T. The “myelodysplastic syndrome / myeloproliferative neoplasm with ring sideroblasts and thrombocytosis (MDS / MPN-RS-T)” in the 2016 WHO classification is renamed MDS / MPN with SF3B1 mutation and thrombocytosis (MDS / MPN- T) in the WHO 2022 classification, and split into two entities in the ICC, represented by MDS / MPN with thrombocytosis and SF3B1 mutation (MDS / MPN-T SF3B1), and MDS / MPN with ring sideroblasts and thrombocytosis, not otherwise specified, in the absence of SF3B1 mutation (MDS / MPN RS-T, NOS). [000101] MDS / MPN with ring sideroblasts and thrombocytosis (MDS-RS-T) in the WHO 2016 classification is characterized by anemia, dysplasia with ring sideroblasts, persistent thrombocytosis ≥450x109 / L and proliferation of large and morphologically atypical megakaryocytes. Several somatic mutations are also associated with MDS-MPN-RS-T, for example, SF3B1, JAK2, and MPL (Montalban-Bravo and Garcia-Manereo. (2020). Best Practice and Research Clinical Hematology; 3(2):101147). In some embodiments, a subject having MDS / MPN-RS-T has co-occurrence of somatic SF3B1 mutations. In some embodiments, a subject having MDS / MPN-RS-T has co-occurrence of somatic SF3B1 mutation with JAK2 V617F mutation. In some embodiments, a subject having MDS / MPN- RS-T has co-occurrence of somatic SF3B1 mutation with CALR or MPL mutations. According to the WHO 2022 classification, the term MDS / MPN-RS-T has been kept to be used for cases with wild-type SF3B1 and ≥15% ring sideroblasts. In contrast, MDS / MPN- RS-T with wildtype SF3B1 mutation is designated “MDS / MPN with sideroblasts and thrombocytosis, NOS” in the ICC. [000102] In some embodiments, diagnosis criteria for MDS / MPN-RS-T, NOS includes thrombocytosis with a platelet count ≥450 × 10⁹ / L and anemia associated with erythroid- lineage dysplasia, with or without multilineage dysplasia, along with ≥15% ring sideroblasts.Blasts are <1% in the peripheral blood and <5% in the bone marrow. The presence of clonality may be demonstrated through cytogenetic abnormalities and / or somatic mutations; in their absence, there may be no recent exposure to cytotoxic or growth factor therapy that could explain the myelodysplastic / myeloproliferative features. There is also absence of SF3B1 mutation, no BCR::ABL1 or genetic abnormalities, of myeloid / lymphoid neoplasms with eosinophilia and tyrosine kinase gene fusions; no t(3;3)(q21.3;q26.2), inv(3) (q21.3q26.2), or del(5q). In some embodiments, a subject described here in does not have MDS / MPN-RS-T, NOS. [000103] In some embodiments, an MDS / MPN overlap syndrome is MDS / MPN-T SF3B1. In some embodiments, a subject having or at risk of developing MDS has or is at risk of developing MDS / MPN-T SF3B1. In some embodiments, a subject described herein does not have MDS / MPN-T SF3B1. MDS / MPN-T SF3B1 is characterized by thrombocytosis and SF3B1 mutation. Other diagnostic criteria include thrombocytosis, with platelet count ≥ 450 × 109 / L; anemia (threshold same as for MDS); blasts < 1% in blood and <5% in bone marrow; presence of SF3B1 mutation (VAF > 10%), isolated or associated with abnormal cytogenetics and / or other myeloid neoplasm-associated mutations; no history of recent cytotoxic or growth factor therapy that could explain the myelodysplastic / myeloproliferative features; no BCR::ABL1 or genetic abnormalities of myeloid / lymphoid neoplasms with eosinophilia and tyrosine kinase gene fusions; no t(3;3)(q21.3;q26.2), inv(3)(q21.3q26.2), or del(5q); and no history of MPN, MDS, or other myelodysplastic / myeloproliferative neoplasm. In some embodiments, an MDS / MPN overlap syndrome is chronic myelomonocytic leukemia. Chronic myelomonocytic leukemia (CMML) is a myeloid stem cell disease characterized by dysplasia of one or more hematopoietic cell lineage, abnormal production and accumulation of monocytes in the peripheral blood and bone marrow, and abnormal production and accumulation of blast in the peripheral blood and bone marrow. CMML can be classified as a classical (i.e., typical) or special (i.e., atypical) variant, depending on diagnostic features; for a review of diagnostic criteria for CMML variants, see Valent et al. (2019). Haematologica. 104(10):1935-1949. Classical (i.e., not a special variant) CMML is defined by persistence of absolute peripheral blood monocytosis (≥1x109 / L for ≥3 months or ≥0.5 × 109 / L) or relative (≥10%) peripheral blood monocytosis; blast count of <19% or < 20% in peripheral blood and / or bone marrow; and exclusion of: BCR-ABL1+ leukemia, APL, MPN, and other hematologic neoplasms which can cause monocytosis. Other diagnostic criteria for CMML include the presence of dysplasia in one or more myeloid lineages, acquired clonal cytogenetic or molecular abnormalities, and abnormal distributionof peripheral blood monocyte subsets. If monocytosis ≥1 × 10⁹ / L, at least one supporting criterion must be present; if monocytosis is between 0.5 and 1 × 10⁹ / L, both dysplasia and clonal abnormalities must be identified. CMML is further classified as myelodysplastic (MD- CMML) or myeloproliferative (MP-CMML) based on a WBC threshold of 13 × 10⁹ / L, and subgrouped as CMML-1 or CMML-2 according to the percentage of blasts and promonocytes in blood and bone marrow. Classical CMML can be classified as CMML-0, CMML-1, and CMML-2 based on increasing blast cell count. Special variants of CMML also exist, depending on various diagnostic features, such as absolute monocyte count in the peripheral blood, concomitant presentation with another disorder (e.g., myeloid neoplasm, lymphoid neoplasm, systemic macrocytosis), and presence of certain somatic mutations or chromosomal abnormalities. Non-limiting examples of special variants of CMML include: oligomonocytic CMML, CMML with concomitant myeloid neoplasm, CMML with concomitant lymphoid / lymphoproliferative neoplasm, systemic mastocytosis with concomitant CMML, and CMML with expression of a molecular MPN driver. CMML, like MDS, can be primary (i.e., de novo) CMML or secondary (e.g.., as a result of a mutagenic event, ); similarly, CMML can evolve into AML. [000104] In some embodiments, a subject having or at risk of developing MDS has or is at risk of developing CMML. In some embodiments, the CMML is classical CMML. In some embodiments, the CMML is CMML-0. In some embodiments, the CMML is CMLL-1. In some embodiments, the CMML is CMML-2. In some embodiments, the CMML is a special variant of CMML. [000105] In some embodiments, based on the presenting WBC count, the French– American–British (FAB) classification distinguished CMML into two subtypes: myeloproliferative CMML (MP-CMML; WBC count ≥ 13 × 109 / L) and myelodysplastic CMML (MD-CMML; WBC count < 13 × 109 / L). In some embodiments, MP-CMML has a poor outcome and a higher rate of AML transformation. In some embodiments, in CMML, the proliferative component is manifested as monocytosis often in association with splenomegaly and / or leukocytosis. In some embodiments, CMML prognosis can be based on the CMML-specific prognostic scoring system–molecular model (CPSS molecular score), which includes the percentage of BM blasts, the FAB subtype of CMML (WBC > 13 × 109 / L), the need for transfusion support, and the presence of genetic markers (ASXL1, RUNX1, NRAS, SETBP1, and cytogenetic abnormalities) as risk factors. In some embodiments, a subject having CMML has mutations in one or more of the following genes:IDH1, RSF2, TET2, ASXL1, SETBP1, NRAS / KRAS, RUNX1, CBL, SRSF2, EZH2, NRAS, CBL, KRAS, NPM1, PTPN11, DNMT3A, ZRSR2, NF1, FLT3 and / or JAK2. [000106] In some embodiments, a subject having CMML has a percentage of peripheral blood monocytes of at least 10% (e.g., at least 10%, at least 12%, at least 15%, at least 18%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, or more) of all leukocytes. In some embodiments, a subject having CMML has a percentage of peripheral blood monocytes in the range of 10%-95% (e.g., 10%-95%, 10%- 90%, 10%-85%, 10%-80%, 10%-75%, 10%-70%, 10%-65%, 10%-60%, 10%-55%, 10%- 50%, 10%-45%, 10%-40%, 10%-35%, 10%-30%, 10%-25%, 10%-20%, 10%-15%, 15%- 95%, 15%-90%, 15%-85%, 15%-80%, 15%-75%, 15%-70%, 15%-65%, 15%-60%, 15%- 55%, 15%-50%, 15%-45%, 15%-40%, 15%-35%, 15%-30%, 15%-25%, 15%-20%, 20%- 95%, 20%-90%, 20%-85%, 20%-80%, 20%-75%, 20%-70%, 20%-65%, 20%-60%, 20%- 55%, 20%-50%, 20%-45%, 20%-40%, 20%-35%, 20%-30%, 20%-25%, 25%-95%, 25%- 90%, 25%-85%, 25%-80%, 25%-75%, 25%-70%, 25%-65%, 25%-60%, 25%-55%, 25%- 50%, 25%-45%, 25%-40%, 25%-35%, 25%-30%, 30%-95%, 30%-90%, 30%-85%, 30%- 80%, 30%-75%, 30%-70%, 30%-65%, 30%-60%, 30%-55%, 30%-50%, 30%-45%, 30%- 40%, 30%-35%, 35%-95%, 35%-90%, 35%-85%, 35%-80%, 35%-75%, 35%-70%, 35%- 65%, 35%-60%, 35%-55%, 35%-50%, 35%-45%, 35%-40%, 40%-95%, 40%-90%, 40%- 85%, 40%-80%, 40%-75%, 40%-70%, 40%-65%, 40%-60%, 40%-55%, 40%-50%, 40%- 45%, 45%-95%, 45%-90%, 45%-85%, 45%-80%, 45%-75%, 45%-70%, 45%-65%, 45%- 60%, 45%-55%, 45%-50%, 50%-95%, 50%-90%, 50%-85%, 50%-80%, 50%-75%, 50%- 70%, 50%-65%, 50%-60%, 50%-55%, 55%-95%, 55%-90%, 55%-85%, 55%-80%, 55%- 75%, 55%-70%, 55%-65%, 55%-60%, 60%-95%, 60%-90%, 60%-85%, 60%-80%, 60%- 75%, 60%-70%, 60%-65%, 65%-95%, 65%-90%, 65%-85%, 65%-80%, 65%-75%, 65%- 70%, 70%-95%, 70%-90%, 70%-85%, 70%-80%, 70%-75%, 75%-95%, 75%-90%, 75%- 85%, 75%-80%, 80%-95%, 80%-90%, 80%-85%, 85%-95%, 85%-90%, or 90%-95%) of all leukocytes. [000107] In some embodiments, a subject having CMML has anemia. In some embodiments, anemia in CMML is due to low numbers of red blood cells. In some embodiments, an anti-HJV antibody described in herein improves anemia in a subject having CMML. In some embodiments, a subject having MDS / MPN has clonal monocytosis of undetermined significance(CMUS). In some embodiments, CC recognizes the CMUS as a precursor of CMML. In some embodiments, a subject having CMUS is characterized bypersistent monocytosis (monocytes ≥ 10% and≥ 0.5 × 109 / L of the WBC), the presence of myeloid neoplasm-associated mutation(s), and the absence of BM morphologic findings of CMML. In some embodiments, a subject with CMUS with cytopenia is characterized as clonal cytopenia and monocytosis of undetermined significance (CCMUS). In some embodiments, an anti-HJV antibody described in herein improves anemia in a subject having CMUS or CCMUS. [000108] In some embodiments, treatment of a subject having or at risk of developing MDS with a therapeutic agent prevents, slows, or reverses evolution to acute myeloid leukemia. Acute myeloid leukemia (AML) is a hematopoietic cell malignancy which results in overproduction of neoplastic clonal myeloid stem cells. AML is characterized by presence of ≥20% blasts in the peripheral blood or bone marrow and / or presence of one or more specific chromosomal abnormalities: t(8;21), inv(16), or t(15;17). Per the 2016 WHO guidelines (Doner et al. (2017) Blood. 129:424-427.), AML is classified into six categories: AML with recurrent genetic abnormalities, AML with myelodysplasia-related changes (AML-MRC), therapy-related myeloid neoplasms, AML not otherwise specified, myeloid sarcoma, and myeloid proliferations related to Down syndrome. Certain cytogenetic and molecular profiles are associated with favorable, intermediate, or adverse prognosis. As used herein, the phrase “evolution to AML” refers to the progression or transformation of MDS in a subject into AML. AML resulting from MDS or an MDS / MPN overlap syndrome is referred to herein as “secondary” AML. Approximately 30% of cases of MDS eventually evolve into AML. Evolution of MDS to AML occurs when blast counts in the bone marrow increase to ≥20% of total nucleated cells in the marrow. Typically, MDS evolution to AML is accompanied by persistence of founding clonal mutations and expansions of a subclone with new, unique mutations. [000109] In some embodiments, a subject having or at risk of developing MDS has a normal karyotype. A karyotype is an individual's complete set of chromosomes. In some embodiments, an individual’s karyotype a laboratory-produced image of a person's chromosomes isolated from an individual cell and arranged in numerical order. A karyotype may be used to look for abnormalities in chromosome number or structure. A subject can be understood to have a “normal” karyotype when a karyotype of the subject shows typical absolute size, position of centromeres, relative size, basic number, number and position of satellites, and GC content of chromosomes for their corresponding sex. A karyotype of a subject may be determined using any method known in the art, for example, as provided byBates, S. E. (2011). Human pluripotent stem cells: Methods and protocols, 177-190 and Campos-Galindo, I. (2020). In Human Reproductive Genetics, pp. 33-48. Academic Press. [000110] In some embodiments, a subject having or at risk of developing MDS has an abnormal karyotype. A subject can be understood to have an abnormal karyotype when one or more chromosomal abnormalities are present. In some embodiments, a chromosomal abnormality comprises a change in absolute size of a chromosome. In some embodiments, a chromosomal abnormality comprises a change in the position of a centromere. In some embodiments, a chromosomal abnormality comprises a difference in relative size of a first chromosome to a second chromosome (e.g., of the same pair). In some embodiments, a chromosomal abnormality comprises a difference in basic number of chromosomes of a subject. In some embodiments, a chromosomal abnormality comprises a difference in the number and position of satellites of a particular chromosome. In some embodiments, a chromosomal abnormality comprises a difference in GC content of a particular chromosome. Non-limiting examples of chromosomal abnormalities include deletions, inversions, translocations, duplications, and aneuploidies (e.g., trisomy, monosomy). In addition to the isolated deletion of 5q identified in MDS-del(5q), several chromosomal abnormalities are associated MDS (see: Zahid, M. F., et al. (2017). International journal of hematology- oncology and stem cell research, 11(3), 231.) and chromosomal profiles are an important component of MDS prognosis scoring (e.g., under IPSS, IPSS-R, or IPSS-M scoring). Recurrent chromosomal abnormalities are present in as many as 70% of cases of primary MDS and in about 90-95% of cases of secondary MDS. In some embodiments, a subject having or at risk of developing MDS comprises a single chromosomal abnormality. In some embodiments, a subject having or at risk of developing MDS comprises a double chromosomal abnormality. [000111] In some embodiments, a subject having or at risk of developing MDS has a complex karyotype. A complex karyotype (CK), as used herein, refers to a karyotype comprising three or more chromosomal abnormalities. Generally, CKs are associated with worse prognosis of MDS and increased rate of evolution to AML (Shahjahani, M. et al. (2019). Oncology Review. 13(1):389.). In some embodiments, a subject having or at risk of developing MDS has a complex karyotype. Up to 30% of primary (e.g., de novo) MDS cases are associated with a complex karyotype. [000112] In some embodiments, chromosomal abnormalities associated with MDS are the result of previous chemotherapy and / or radiotherapy, such that the subject has secondary MDS. In some embodiments, chromosomal abnormalities associated with MDS are de novomutations not associated with previous chemotherapy or radiotherapy, such that the subject has primary MDS. [000113] Exemplary chromosomal abnormalities associated with MDS include but are not limited to: deletion of 3q (del(3q)), inversion of chromosome 3 (Inv3q), translocation of portions of chromosome 3 (t(3;3)(q21;q26)), monosomy of chromosome 7 (-7), deletion of 7q (del(7q)), trisomy 8 (+8), deletion of 11q (del(11q), deletion of 12p (del(12p)), trisomy 13 (+13), deletion of 13q (del(13q), isochromosome 17q (i(17q), trisomy 19 (+19), deletion of 20q (del20q), trisomy 21 (+21), monosomy 21 (-21), acquired loss of the X chromosome in females (-X), and acquired loss of the Y chromosome in males (-Y). [000114] In some embodiments, a subject having or at risk of developing MDS has a chromosome 3 abnormality. MDS-associated chromosome 3 abnormalities include, for example, deletions, translocations, and inversions of chromosome 3 (inv(3q)). Commonly affected regions of chromosome 3 in MDS include the 3q21 and 3q26 locus (e.g., t(3;3)(q21;q26)). Chromosome 3 abnormalities are rare in MDS. In some embodiments, a subject having or at risk of developing MDS has a chromosome 3 abnormality. In some embodiments, the chromosome 3 abnormality is del(3q). In some embodiments, the chromosome 3 abnormality is an inversion. In some embodiments, the inversion is inv(3q). In some embodiments, the chromosome 3 abnormality is a translocation. In some embodiments, the translocation is t(3;3)(q21;q26). [000115] In some embodiments, a subject having or at risk of developing MDS has a chromosome 7 abnormality. MDS-associated chromosome 7 abnormalities include, for example, monosomy of chromosome 7 (-7) or deletion on 7q. Commonly deleted regions of chromosome 7 in MDS include position 7q22, 7q32-33, and 7q35-36. Chromosome 7 abnormalities have been reported in approximately 10% of cases of primary MDS and up to 50% of cases of secondary MDS. Chromosome 7 abnormalities occur frequently with other cytogenic aberrations and are associated with poor prognosis and high rates of evolution to AML. In some embodiments, a subject having or at risk of developing MDS has a chromosome 7 abnormality. In some embodiments, the chromosome 7 abnormality is -7. In some embodiments, the chromosome 7 abnormality is del(7q). In some embodiments, del(7q) comprises deletion of 7q22. In some embodiments, del(7q) comprises deletion of 7q32-33. In some embodiments, del(7q) comprises deletion of 7q35-36. [000116] In some embodiments, a subject having or at risk of developing MDS has a chromosome 8 abnormality. MDS-associated chromosome 8 abnormalities include, for example, trisomy 8 (+8). Chromosome 8 abnormalities have been reported in approximately5% of cases of MDS. In some embodiments, a subject having or at risk of developing MDS has a chromosome 8 abnormality. In some embodiments, the chromosome 8 abnormality is +8. [000117] In some embodiments, a subject having or at risk of developing MDS has a chromosome 11 abnormality. MDS-associated chromosome 11 abnormalities include, for example, deletions of chromosome 11 (del(11q)). Commonly affected regions of chromosome 11 deletions in MDS include 11q14, 11q23, 11q13q23, and 11q21q23. In some embodiments, a subject having or at risk of developing MDS has a chromosome 11 abnormality. In some embodiments, the chromosome 11 abnormality is del(11q). In some embodiments, del(11q) comprises deletion of 11q14. In some embodiments, del(11q) comprises deletion of 11q23. In some embodiments, del(11q) comprises deletion of 11q13q23. In some embodiments, del(11q) comprises deletion of 11q21q23. [000118] In some embodiments, a subject having or at risk of developing MDS has a chromosome 12 abnormality. MDS-associated chromosome 12 abnormalities include, for example, deletion of 12 (del(12p). A commonly affected region of chromosome 12 deletions in MDS is 12p13. In some embodiments, a subject having or at risk of developing MDS has a chromosome 12 abnormality. In some embodiments, the chromosome 12 abnormality is del(12p). In some embodiments, the chromosome 12 abnormality is del(12p13). [000119] In some embodiments, a subject having or at risk of developing MDS has a chromosome 13 abnormality. MDS-associated chromosome 13 abnormalities include, for example, trisomy (13+) or deletion (del(13q). +13 has been reported in about 0.2% of MDS patients but is strongly associated with evolution to AML. del(13q) has been reported in about 2% of MDS patients. In some embodiments, a subject having or at risk of developing MDS has a chromosome 13 abnormality. In some embodiments, the chromosome 13 abnormality is +13. In some embodiments, the chromosome 13 abnormality is del(13q). [000120] In some embodiments, a subject having or at risk of developing MDS has a chromosome 17 abnormality. MDS-associated chromosome 17 abnormalities include, for example, isochromosome 17 (i(17q)). i(17q) is associated with specific phenotypes, for example, profound anemia, neutrophil morphology changes, and hyperplastic bone marrow. Chromosome 17 abnormalities occur in about 2% of primary MDS cases and in about 4.5% of secondary MDS. Prospective studies find a higher risk for evolution to AML in patients with MDS and a chromosome 17 abnormality. In some embodiments, a subject having or at risk of developing MDS has a chromosome 17 abnormality. In some embodiments, the chromosome 17 abnormality is i(17q).[000121] In some embodiments, a subject having or at risk of developing MDS has a chromosome 19 abnormality. MDS-associated chromosome 19 abnormalities include, for example, trisomy 19 (+19). +19 is strongly associated with de novo myeloid disorders, including MDS and AML. The effect of +19 on MDS prognosis is unknown. In some embodiments, a subject having or at risk of developing MDS has a chromosome 19 abnormality. In some embodiments, the chromosome 19 abnormality is +19. [000122] In some embodiments, a subject having or at risk of developing MDS has a chromosome 20 abnormality. MDS-associated chromosome 20 abnormalities include, for example, deletions (del(20q)). A commonly affected region of chromosome 20 abnormalities in MDS is 20q11. Chromosome 20 abnormalities occur in about 5% of primary MDS cases. Prognosis for MDS patients with chromosome 20 abnormalities, in the absence of complex karyotypes, is generally favorable. In some embodiments, a subject having or at risk of developing MDS has a chromosome 20 abnormality. In some embodiments, the chromosome 20 abnormality is del(20q). In some embodiments, the chromosome 20 abnormality is del(20q11). [000123] In some embodiments, a subject having or at risk of developing MDS has a chromosome 21 abnormality. MDS-associated chromosome 21 abnormalities include, for example, trisomy (+21) or monosomy (-21). In addition to its role in Down’s syndrome, +21 is associated with an increased risk of AML and acute lymphoblastic leukemia; hence, though +21 occurs rarely in MDS patients (about 0.3-0.8% of cases), prospective studies find a higher risk for evolution to AML. -21 is very rare (about 0.3-0.5% of cases), and its effects on prognosis are unknown. In some embodiments, a subject having or at risk of developing MDS has a chromosome 21 abnormality. In some embodiments, the chromosome 21 abnormality is +21. In some embodiments, the chromosome 21 abnormality is -21. [000124] In some embodiments, a subject having or at risk of developing MDS has a sex chromosome abnormality. MDS-associated sex chromosome abnormalities include, for example, acquired losses of a sex chromosome (-X in females, -Y in males). In some embodiments, -X or -Y has been observed to be associated with MDS progression and prognosis. In some embodiments, -X to be associated with an intermediate prognosis is more often associated with a good prognosis, but a 3.8-fold increase in risk. In some embodiments, a subject having or at risk of developing MDS has a sex chromosome abnormality. In some embodiments, the sex chromosome abnormality is -X. In some embodiments, the sex chromosome abnormality is -Y.[000125] In some embodiments, a subject having or at risk of developing MDS has one or more somatic mutations. A somatic mutation is any change in the DNA sequence of a given gene of a somatic cell (e.g., any cell which is not a gamete, germ cell, or gametocyte). Somatic mutations may be inherited or de novo mutations, for example, as the result of endogenous factors, or contact with mutagens. [000126] Several somatic mutations are associated with MDS. In some embodiments, a subject having MDS or is at risk of developing MDS, including both those with normal karyotypes and those with abnormal karyotypes, have at least one point mutation one gene. In some embodiments, a subject having MDS or is at risk of developing MDS, including both those with normal karyotypes and those with abnormal karyotypes, has mutations in 2 or more genes. Non-limiting examples of somatic mutations associated with MDS include, for example, SF3B1, TET2, ASXL1, RUNX1, TP53, DNMT3A, EZH2, SRSF2, NRAS, JAK2, ETV6, U2AF1, CBL, IDH2, ZRSR2, NPM1, STAG2, IDH1, KRAS, GNAS, PTPN11, SETBP1, BRAF, PTEN, CDKN2A, FLT3, and MLL. [000127] In some embodiments, a subject having or at risk of developing MDS has an SF3B1 mutation. SF3B1 is a gene encoding splicing factor 3B subunit 1 (SF3B1), a subunit of a splicing factor complex involved in the recognition and assembly of spliceosomes. Mutations in SF3B1 are associated with lymphocytic leukemia, MDS (e.g., RARS, RARS-T), and breast cancer. SF3B1 mutations are also associated with iron overload in MDS patients, as well as MDS-RS. In some embodiments, a subject having or at risk of developing MDS does not have an SF3B1 mutation. [000128] In some embodiments, a subject having or at risk of developing MDS has a TET2 mutation. TET2 is a gene encoding Tet methylcytosine dioxygenase 2 (TET2), a protein that catalyzes conversion of the DNA base methylcytosine to 5- hydroxymethylcytosine, and which forms a complex with mixed lineage leukemia 1 (MLL) to act as a transcription factor. Mutations in TET2 are associated with MDS, MPN, CMML, and AML. TET2 mutations are often associated with chromosomal abnormalities. some embodiments, a subject having or at risk of developing MDS does not have a TET2 mutation. [000129] In some embodiments, a subject having or at risk of developing MDS has an ASXL1 mutation. ASXL1 is a gene encoding additional sex combs-like protein 1 (ASXL1), a regulator of chromatin remodeling which interacts with homeobox (HOX) genes. Mutations in ASXL1 are associated with MDS and CMML; ASXL1 mutations are also associated with a worse prognosis in MDS. In some embodiments, a subject having or at risk of developing MDS does not have an ASXL1 mutation.[000130] In some embodiments, a subject having or at risk of developing MDS has a RUNX1 mutation. RUNX1 is a gene encoding runt-related transcription factor 1 (RUNX1), also known as acute myeloid leukemia 1 protein (AML1) and core-binding factor subunit alpha-2 (CBFA2), a transcription factor involved in differentiation of hematopoietic stem cells into mature blood cells. Mutations in RUNX1 are associated with several types of leukemia, breast cancer, bleeding disorders, MDS, and various myeloid malignancies. RUNX1 mutations are also associated with a worse prognosis in MDS. In some embodiments, a subject having or at risk of developing MDS does not have a RUNX1 mutation. [000131] In some embodiments, a subject having or at risk of developing MDS has a TP53 mutation. TP53 is a gene encoding tumor protein p53 (TP53), also known as cellular tumor antigen p53 (p53) or transformation-related protein 53 (TRP53), a regulatory protein involved in mediating progression of a cell through the cell cycle, initiating apoptosis, and activating DNA repair. Mutations in TP53 are associated with many proliferative disorders, including leukemia and myeloproliferative disorders. TP53 mutations are often associated with chromosomal abnormalities and are strong predictors of poor MDS prognosis. In some embodiments, a subject having or at risk of developing MDS does not have a TP53 mutation. [000132] In some embodiments, a subject having or at risk of developing MDS has a DNMT3A mutation. DNMT3A is a gene encoding DNA (cytosine-5)-methyltransferase 3A (DNMT3A), an enzyme that catalyzes DNA methylation . Mutations in DNMT3A are associated with clonal hematopoiesis and several cancers, such as AML. In some embodiments, a subject having or at risk of developing MDS does not have a DNMT3A mutation. [000133] In some embodiments, a subject having or at risk of developing MDS has an EZH2 mutation. EZH2 is a gene encoding enhancer of zeste homolog 2 (EZH2), a histone- lysine N-methyltransferase enzyme involved in histone methylation and transcriptional repression. Mutations in EZH2 are involved in multiple cancers and in dysfunctions of hematopoiesis, including MDS. In some embodiments, a subject having or at risk of developing MDS does not have an EZH2 mutation. [000134] In some embodiments, a subject having or at risk of developing MDS has an SRSF2 mutation. SRSF2 is a gene encoding splicing factor, arginine / serine-rich 2 (SRSF2), a splicing factor involved in mRNA splicing and export from the nucleus. Mutations in SRSF2 are associated with aberrant hematopoiesis, including MDS. In some embodiments, a subject having or at risk of developing MDS does not have an SRSF2 mutation.[000135] In some embodiments, a subject having or at risk of developing MDS has a NRAS mutation. NRAS is a gene encoding neuroblastoma rat sarcoma virus (Ras) (N-RAS), a regulator of cell division and differentiation. Mutations in NRAS are associated with several proliferative disorders, including leukemia, melanoma, MDS, AML, and MPN. In some embodiments, a subject having or at risk of developing MDS does not have a NRAS mutation. [000136] In some embodiments, a subject having or at risk of developing MDS has a JAK2 mutation. JAK2 is a gene encoding Janus kinase 2 (JAK2), a non-receptor tyrosine kinase involved in cytokine signaling, Mutations in JAK2 are associated with leukemia and myeloproliferative disorders, such as MDS. In some embodiments, a subject having or at risk of developing MDS does not have a JAK2 mutation. [000137] In some embodiments, a subject having or at risk of developing MDS has an ETV6 mutation. ETV6 is a gene encoding translocation-Ets-leukemia virus (ETV6), also known as TEL, a protein involved in the development and growth of hematological cells. Mutations in ETV6 are associated with thrombocytopenia and hematological cancers, such as CML, AML, MDS, and multiple myeloma. In some embodiments, a subject having or at risk of developing MDS does not have an ETV6 mutation. [000138] In some embodiments, a subject having or at risk of developing MDS has a U2AF1 mutation. U2AF1 is a gene encoding U2 Small Nuclear RNA Auxiliary Factor 1 (U2AF1), a non-snRNP protein and subunit of the U2 auxiliary splicing factor associated with constitutive and enhancer-dependent RNA splicing. Mutations in U2AF1 are associated with MDS and uterine carcinosarcoma. In some embodiments, a subject having or at risk of developing MDS does not have a U2AF1 mutation. [000139] In some embodiments, a subject having or at risk of developing MDS has a CBL mutation. CBL is a gene encoding Casitas B-lineage lymphoma (CBL), an E3 ubiquitin- protein ligase involved in receptor tyrosine kinase signaling. Mutations in CBL are associated with myeloproliferative disorders, including MDS and AML. In some embodiments, a subject having or at risk of developing MDS does not have a CBL mutation. [000140] In some embodiments, a subject having or at risk of developing MDS has an IDH2 mutation. IDH2 is a gene encoding isocitrate dehydrogenase, mitochondrial (IDH2), a catalyst of oxidative decarboxylation of isocitrate to 2-oxoglutarate and is involved in intermediary metabolism and energy production. Mutations in IDH2 are associated with several diseases, including those of the brain, heart, and proliferative disorders including gliomas, lymphoma, AML, MDS, and connective syndromes. In some embodiments, a subject having or at risk of developing MDS does not have an IDH2 mutation.[000141] In some embodiments, a subject having or at risk of developing MDS has a ZRSR2 mutation. ZRSR2 is a gene encoding zinc finger CCH-type, RNA Binding Motif and Serine / Arginine Rich 2 (ZRSR2), also known as U2 small nuclear ribonucleoprotein auxiliary factor 35 kDa subunit-related protein 2 (U2AF1RS2), an essential splicing factor involved in spliceosome assembly. Mutations in ZRSR2 are involved in myeloproliferative disorders, including MDS. In some embodiments, a subject having or at risk of developing MDS does not have a ZRSR2 mutation. [000142] In some embodiments, a subject having or at risk of developing MDS has an NPM1 mutation. NPM1 is a gene encoding nucleophosmin 1 (NPM1), also known as nucleolar phosphoprotein B23 or numatrin, a molecular chaperone for proteins transported into the nucleolus and is involved in the biogenesis of ribosomes. Mutations in NPM1 are involved in several proliferative disorders, including lymphomas, leukemias, and MDS. In some embodiments, a subject having or at risk of developing MDS does not have an NPM1 mutation. [000143] In some embodiments, a subject having or at risk of developing MDS has a STAG2 mutation. STAG2 is a gene encoding cohesin subunit SA-2 (STAG2), also known as SA2, a subunit of the Cohesin complex and is involved in sister chromatid cohesion and DNA looping during anaphase. Mutations in STAG2 are involved in several proliferative disorders, including non-muscle-invasive bladder cancer and MDS. In some embodiments, a subject having or at risk of developing MDS does not have a STAG2 mutation. [000144] In some embodiments, a subject having or at risk of developing MDS has an IDH1 mutation. IDH1 is a gene encoding isocitrate dehydrogenase (IDH1), an enzyme which catalyzes oxidative decarboxylation of isocitrate to 2-oxoglutarate as part of glucose metabolism. Mutations in IHD1 are associated with the development of brain tumors (e.g., gliomas, astrocytomas, oligodendroglioma), AML, and MDS. In some embodiments, a subject having or at risk of developing MDS does not have an IDH1 mutation. [000145] In some embodiments, a subject having or at risk of developing MDS has a KRAS mutation. KRAS is a gene encoding Kirsten Ras (K-RAS), a GTPase involved in the Ras / MAPK pathway. Mutations in KRAS are associated with several proliferative disorders, including lung cancers, colorectal cancers, pancreatic cancers, and MDS. In some embodiments, a subject having or at risk of developing MDS does not have a KRAS mutation. [000146] In some embodiments, a subject having or at risk of developing MDS has a GNAS mutation. GNAS is a gene encoding several guanine nucleotide binding protein, alpha stimulating activity (GNAS) polypeptides, which are involved in signal transduction ofadenylyl cyclase activity. Mutations in GNAS are associated with metabolic disorders and several proliferative disorders, including connective tissue cancers, and MDS. In some embodiments, a subject having or at risk of developing MDS does not have a GNAS mutation. [000147] In some embodiments, a subject having or at risk of developing MDS has a PTPN11 mutation. PTPN11 is a gene encoding protein tyrosine phosphatase non-receptor type 11 (PTPN11), also known as Src homology region 2 domain-containing phosphatase-2 (SHP-2), a signaling molecule involved in the MAPK pathway. Mutations in PTPN11 are associated with several types of tumors and proliferative disorders (e.g., MDS). In some embodiments, a subject having or at risk of developing MDS does not have a PTPN11 mutation. [000148] In some embodiments, a subject having or at risk of developing MDS has a STEBP1 mutation. SETBP1 is a gene encoding SET binding protein 1 (SETBP1), a DNA- binding protein involved in histone methylation. Mutations in SETBP1 are associated with CMML and MDS. In some embodiments, a subject having or at risk of developing MDS does not have a STEBP1 mutation. [000149] BRAF is a gene encoding V-raf murine sarcoma viral oncogene homolog B (BRAF), a serine / threonine protein kinase involved in MAPK / ERK signaling. Mutations in BRAF are associated with several proliferative disorders (e.g., MDS) and developmental disorders known as RASopathies. In some embodiments, a subject having or at risk of developing MDS does not have a BRAF mutation. [000150] In some embodiments, a subject having or at risk of developing MDS has a PTEN mutation. PTEN is a gene encoding phosphatase and tensin homolog (PTEN), a tumor suppressor protein involved in cell cycle regulation and inhibition of the Akt signaling pathway. Mutations in PTEN are involved in proliferative disorders (e.g., MDS), non- cancerous neoplasia, and neurodevelopmental disorders. In some embodiments, a subject having or at risk of developing MDS does not have a PTEN mutation. [000151] In some embodiments, a subject having or at risk of developing MDS has a CDKN2A mutation. CDKN2A is a gene encoding two cyclin-dependent kinase inhibitor 2A proteins, p16 and p14arf, two members of the INK4 family which mediate CDK4 signaling and p53 activation, respectively. Mutations in CDKN2A are associated with several proliferative disorders, including lymphomas, carcinomas, melanoma, and myeloproliferative neoplasms. In some embodiments, a subject having or at risk of developing MDS does not have a CDKN2A mutation.[000152] In some embodiments, a subject having or at risk of developing MDS has an FLT3 mutation. FLT3 is a gene encoding FMS-like tyrosine kinase III, a transmembrane tyrosine kinase. FLT3 is involved in signaling related to Stat5, RAS, and PI3 kinase and is important for normal hematopoiesis. Mutations in FLT3 are associated with several clonal hematopoietic disorders, including, for example, AML, CMML, and MDS. MDS is particularly associated with MDS-EB and, more broadly, with intermediate MDS. In some embodiments, a subject having or at risk of developing MDS does not have an FLT3 mutation. [000153] In some embodiments, a subject having or at risk of developing MDS has an MLL mutation. MLL, also known as KMT2A, ALL-1, and HRX, is a gene encoding mixed- lineage leukemia 1 (MLL1), also known as lysine[K]-specific methyltransferase 2A (KMT2A). MLL1 is a histone modifying enzyme involved in transcriptional regulation and is an important regulator of epiblast-derived stem cells. Mutations of MLL are associated with neurological disorders, aggressive acute leukemia, including AML (5-10% of AML patients), and MDS (5-6% of MDS patients), where its presence is associated with a poor prognosis. In some embodiments, a subject having or at risk of developing MDS does not have an MLL mutation. [000154] In some embodiments, MDS can be categorized using International Prognostic Scoring System (IPSS) (see, e.g., THE INTERNATIONAL PROGNOSTIC SCORING SYSTEM, lls.org / myelodysplastic-syndromes / diagnosis / international-prognostic-scoring- system). In some embodiments, the present disclosure provides composition (e.g., an anti- HJV antibody) and methods for treating a subject having low risk MDS according to International Prognostic Scoring System (IPSS). In some embodiments, the present disclosure provides composition (e.g., an anti-HJV antibody) and methods for treating a subject having intermediate (e.g., intermediate-1 or intermediate-2) risk MDS according to IPSS. In some embodiments, the present disclosure provides composition (e.g., an anti-HJV antibody) and methods for treating a subject having high risk MDS according to IPSS. IPSS uses three indicators to predict the course of MDS in a subject, including: (i) the percentage of leukemic blast cells in the marrow (e.g., less than 5 = 0 points; 5 to10 = 0.5 points; 11 to 20 = 1.5 points; and 21 to 30 = 2 points); (ii) the type of chromosomal changes, if any, in the marrow cells (cytogenetics) (e.g., none, del(5q), del(20q) = 0 points; 3 or more abnormalities, abnormal chromosome 7 = 1 point; and other abnormalities = 0.5 points); (iii) the presence of one or more low blood cell counts (cytopenias such as anemia, neutropenia or thrombocytopenia)(e.g., none or 1 = 0 points; 2 or 3 = 0.5 points). In some embodiments, asubject has low risk MDS according to IPSS. In some embodiments, a subject having low risk MDS according to IPSS has an IPSS Total Risk Score of 0 points. In some embodiments, a subject has intermediate-1 risk MDS according to IPSS. In some embodiments, a subject having intermediate-1 risk MDS according to IPSS has an IPSS Total Risk Score in the range of 0.5 to 1 point (e.g., 0.5 point or 1 point). In some embodiments, a subject has intermediate- 2 risk MDS according to IPSS. In some embodiments, a subject having intermediate-2 risk MDS according to IPSS has an IPSS Total Risk Score in the range of 1.5 to 2 point (e.g., 1.5 points, or 2 points). In some embodiments, a subject has high risk MDS according to IPSS. In some embodiments, a subject having high risk MDS according to IPSS has an IPSS Total Risk Score of 2.5 or more points (e.g., at least 2.5 points, at least 3 points, at least 3.5 points, at least 4 points, at least 4.5 points, at least 5 points, at least 5.5 points, at least 6 points, at least 6.5 points, at least 7 points, at least 7.5 points, at least 8 points, at least 8.5 points, at least 9 points, at least 9.5 points, at least 10 points, or more). [000155] In some embodiments, MDS can be categorized using International Prognostic Scoring System-Revised (IPSS-R) (see, e.g., THE INTERNATIONAL PROGNOSTIC SCORING SYSTEM, lls.org / myelodysplastic- syndromes / diagnosis / international-prognostic-scoring-system). In some embodiments, the present disclosure provides composition (e.g., an anti-HJV antibody) and methods for treating a subject having very low risk MDS according to International Prognostic Scoring System- Revised (IPSS-R). In some embodiments, the present disclosure provides composition (e.g., an anti-HJV antibody) and methods for treating a subject having low risk MDS according to IPSS-R. In some embodiments, the present disclosure provides composition (e.g., an anti- HJV antibody) and methods for treating a subject having intermediate risk MDS according to IPSS-R. In some embodiments, the present disclosure provides composition (e.g., an anti- HJV antibody) and methods for treating a subject having high risk MDS according to IPSS- R. In some embodiments, the present disclosure provides composition (e.g., an anti-HJV antibody) and methods for treating a subject having very high risk MDS according to IPSS-R. IPSS-R uses five indicators to predict the course of MDS in a subject, including: (i) the percentage of blast cells in the bone marrow (e.g., less than or equal to 2 = 0 points; Grater than 2 to less than 5 = 1 point; 5 to 10 = 2 points; Greater than 10 = 3 points); (ii) cytogenetic (i.e., chromosomal changes) (e.g., -Y, del(11q) = 0 points; normal, del(5q), del(12p), del(20q), double including del(51) = 1 point; del(71), +8, +19, i(17q), any other single or double independent clone = 2 points; -7, inv(3), +(3q), del(3q), double including -7 / del(7q), complex:3 abnormalities = 3 points; more than 3 abnormalities = 4 points); (iii) hemoglobinconcentration (g / dL) (e.g., equal to or greater than 10 = 0 points; 8 to less than 10 = 1 point; less than 8 = 1.5 points); (iv) platelet count (x109 / L of blood) (e.g., equal to or greater than 100 = 0 points; 50 to less than 100 = 0.5 points; less than 50 = 1 point); and (v) Absolute neutrophil count(x109 / L of blood)(e.g., equal to or greater than 0.8 = 0 points; less than 0.8 = 0.5 points). In some embodiments, a subject has very low risk MDS according to IPSS-R. In some embodiments, a subject having very low risk MDS according to IPSS-R has an IPSS-R Total Risk Score of 1.5 or less points (e.g., 1.5 points, 1 points, 0.5 points, or 0 points). In some embodiments, a subject has low risk MDS according to IPSS-R. In some embodiments, a subject having low risk MDS according to IPSS-R has an IPSS Total Risk Score of 2-3 points (e.g., 2 points, 2.5 points, or 3 points). In some embodiments, a subject has intermediate risk MDS according to IPSS-R. In some embodiments, a subject having intermediate risk MDS according to IPSS-R has an IPSS-R Total Risk Score in the range of 3.5-4.5 points (e.g., 3.5 points, 4 points, or 4.5 points). In some embodiments, a subject has high risk MDS according to IPSS-R. In some embodiments, a subject having high risk MDS according to IPSS-R has an IPSS-R Total Risk Score of 5-6 points (e.g., 5 points, 5.5 points, or 6 points). In some embodiments, a subject has very high risk MDS according to IPSS-R. In some embodiments, a subject having very high risk MDS according to IPSS-R has an IPSS-R Total Risk Score of 6.5 or more points (e.g., 6.5 points, 7 points, 7.5 points, 8 points, 8.5 points, 9 points, 9.5 points, 10 points, 6.5-10 points, 6.5-9.5 points, 6.5-9 points, 6.5-8.5 points, 6.5-8 points, 6.5-7.5 points, 6.5-7 points, 7-10 points, 7-9.5 points, 7-9 points, 7-8.5 points, 7-8 points, 7-7.5 points, 7.5-10 points, 7.5-9.5 points, 7.5-9 points, 7.5-8.5 points, 7.5- 8 points, 8-10 points, 8-9.5 points, 8-9 points, 8-8.5 points, 8.5-10 points, 8.5-9.5 points, 8.5- 9 points, 8-8.5 points, 9-10 points, 9-9.5 points, or 9.5-10 points). [000156] In some embodiments, MDS can be categorized using International Prognostic Scoring System-Molecular (IPSS-M) (see, e.g., Bernard et al., Molecular International Prognostic Scoring System for Myelodysplastic Syndromes, NEJM Evid 2022; 1 (7)). IPSS- M categorizes MDS by combining clinical parameters (e.g., percent of bone marrow blasts, platelets count, and hemoglobin), cytogenetic abnormalities (same as IPSS-R cytogenetic category), and somatic mutations of 31 genes (e.g., 16 prognostic genes such as ASXL1, CBL, DNMT3A, ETV6, EZH2, FLT3, IDH2, KRAS, MLLPTD, NPM1, NRAS, RUNX1, SF3B15q, SF3B1α, SRSF2, TP53multihit, and U2AF1; and a residual group of 15 genes including BCOR, BCORL1, CEBPA, ETNK1, GATA2, GNB1, IDH1, NF1, PHF6, PPM1D, PRPF8, PTPN11, SETBP1, STAG2, and WT1). IPSS-M score can be calculated by suitable methods, e.g., web calculator: mds-risk-model.com. In some embodiments, the presentdisclosure provides composition (e.g., an anti-HJV antibody) and methods for treating a subject having very low risk MDS according to IPSS-M. In some embodiments, the present disclosure provides composition (e.g., an anti-HJV antibody) and methods for treating a subject having low risk MDS according to IPSS-M. In some embodiments, the present disclosure provides composition (e.g., an anti-HJV antibody) and methods for treating a subject having moderate low risk MDS according to IPSS-M. In some embodiments, the present disclosure provides composition (e.g., an anti-HJV antibody) and methods for treating a subject having moderate high risk MDS according to IPSS-M. In some embodiments, the present disclosure provides composition (e.g., an anti-HJV antibody) and methods for treating a subject having high risk MDS according to IPSS-M. In some embodiments, the present disclosure provides composition (e.g., an anti-HJV antibody) and methods for treating a subject having very high risk MDS according to IPSS-M. In some embodiments, a subject has very low risk MDS according to IPSS-M. In some embodiments, a subject having very low risk MDS according to IPSS-M has an IPSS-R Total Risk Score of -1.5 or less points (e.g., less than -1.5 points, less than -1.5 points, less than -1.6 points, less than -1.7 points, less than -1.8 points, less than -1.9 points, less than -2.0 points, less than -2.1 points, less than -2.2 points, less than -2.3 points, less than -2.4 points, less than -2.5 points, less than -2.6 points, less than -2.7 points, less than -2.8 points, less than -2.9 points, less than -3 points, less than -3.1 points, less than -3.2 points, less than -3.3 points, less than -3.4 points, less than -3.5 points, less than -3.6 points, less than -3.7 points, less than -3.8 points, less than -3.9 points, less than -4 points, less than -4.1 points, less than -4.2 points, less than -4.3 points, less than -4.4 points, less than -4.5 points, less than -4.6 points, less than -4.7 points, less than -4.8 points, less than -4.9 points, or less than 5 points). In some embodiments, a subject has low risk MDS according to IPSS-M. In some embodiments, a subject having low risk MDS according to IPSS-M has an IPSS-M Total Risk Score in the range of -1.5 to -0.5 points (e.g.,-1.5 to -0.5 points, -1.5 to -0.6 points, -1.5 to -0.7 points, -1.5 to -0.8 points, -1.5 to -0.9 points, -1.5 to -1 points, -1.5 to -1.1 points, -1.5 to -1.2 points, -1.5 to -1.3 points, -1.5 to -1.4 points, -1.2 to -0.5 points, -1.2 to -0.6 points, -1.2 to -0.7 points, -1.2 to -0.8 points, -1.2 to - 0.9 points, -1.2 to -1 points, -1.2 to -1.1 points, -1 to -0.5 points, -1 to -0.6 points, -1 to -0.7 points, -1 to -0.8 points, -1 to -0.9 points, -0.8 to -0.5 points, -0.8 to -0.6 points, -0.8 to -0.5 points, or -0.6 to -0.5 points). In some embodiments, a subject has moderate low risk MDS according to IPSS-M. In some embodiments, a subject having moderate low risk MDS according to IPSS-M has an IPSS-M Total Risk Score in the range of -0.5 to 0 points (e.g., - 0.5 to 0 points, -0.5 to -0.1 points, -0.5 to -0.2 points, -0.5 to -0.3 points, -0.5 to -0.4 points, -0.4 to 0 points, -0.4 to -0.1 points, -0.4 to -0.2 points, -0.4 to -0.3 points, -0.3 to 0 points, -0.3 to -0.1 points, -0.3 to -0.2 points, -0.2 to 0 points, -0.2 to -0.1 points, -0.1 to 0 points). In some embodiments, a subject has moderate high risk MDS according to IPSS-M. In some embodiments, a subject having moderate high risk MDS according to IPSS-M has an IPSS-M Total Risk Score in the range of 0 to 0.5 points (e.g., 0 to 0.5 points, 0 to 0.4 points, 0 to 0.3 points, 0 to 0.2 points, 0 to 0.1 points, 0.1 to 0.5 points, 0.1 to 0.4 points, 0.1 to 0.3 points, 0.1 to 0.2 points, 0.2 to 0.5 points, 0.2 to 0.4 points, 0.2 to 0.3 points, 0.3 to 0.5 points, 0.3 to 0.4 points, or 0.4 to 0.5 points). [000157] In some embodiments, a subject has high risk MDS according to IPSS-M. In some embodiments, a subject having high risk MDS according to IPSS-M has an IPSS-M Total Risk Score in the range of 0.5 to 1.5 points (e.g., 0.5 to 1.5 points, 0.5 to 1.4 points, 0.5 to 1.3 points, 0.5 to 1.2 points, 0.5 to 1.1 points, 0.5 to 1 points, 0.5 to 0.9 points, 0.5 to 0.8 points, 0.5 to 0.7 points, 0.5 to 0.6 points, 0.8 to 1.5 points, 0.8 to 1.4 points, 0.8 to 1.3 points, 0.8 to 1.2 points, 0.8 to 1.1 points, 0.8 to 1 points, 0.8 to 0.9 points, 1 to 1.5 points, 1 to 1.4 points, 1 to 1.3 points, 1 to 1.2 points, 1 to 1.1 points, 1.2 to 1.5 points, 1.2 to 1.4 points, or 1.2 to 1.3 points). In some embodiments, a subject has very high risk MDS according to IPSS-M. In some embodiments, a subject having very high risk MDS according to IPSS-M has an IPSS-M Total Risk Score of more than 1.5 points (e.g., more than 1.5 points, more than 1.8 points, more than 2 points, more than 2.5 points, more than 3 points, more than 3.5 points, more than 4 points, more than 4.5 points, more than 5 points, more than 6 points, more than 7 points, more than 8 points, more than 9 points, more than 10 points, or more). In some embodiments, a subject having very high risk MDS according to IPSS-M has an IPSS- M Total Risk Score of more than 1.5 points (e.g., in the range of 1.6-10 points, 1.6-9 points, 1.6-8 points, 1.6-7 points, 1.6-6 points, 1.6-5 points, 1.6-4 points, 1.6-3 points, 1.6-2 points, 1.6-1.9 points, 1.6-1.8 points, 1.6-1.7 points, 1.8-10 points, 1.8-9 points, 1.8-8 points, 1.8-7 points, 1.8-6 points, 1.8-5 points, 1.8-4 points, 1.8-3 points, 1.8-1.9 points, 1.8-2 points, 2-10 points, 2-9 points, 2-8 points, 2-7 points, 2-6 points, 2-5 points, 2-4 points, 2-3 points, 3-10 points, 3-9 points, 3-8 points, 3-7 points, 3-6 points, 3-5 points, 3-4 points, 4-10 points, 4-9 points, 4-8 points, 4-7 points, 4-6 points, 4-5 points, 5-10 points, 5-9 points, 5-8 points, 5-7 points, 5-6 points, 6-10 points, 6-9 points, 6-8 points, 6-7 points, 7-10 points, 7-9 points, 7-8 points, 8-10 points, 8-9 points, or 9-10 points). In some embodiments, a subject having MDS (e.g., any MDS categories described herein) is functionally iron deficient. Functional iron deficiency (FID) or functionally iron deficient refers to a state of iron-restricted erythropoiesis characterized by an imbalance between iron demand and serum iron that isreadily available for effective erythropoiesis. Typically, of the total iron in an individual’s body, part of it is contained in the hemoglobin needed to carry oxygen through the blood, and most of the rest is contained in ferritin complexes that are present in all cells, but most common in bone marrow, liver, and spleen (Cellular Iron Store). In some embodiments, the liver stores of ferritin are the primary physiologic source of reserve iron in the body. In subjects with FID, iron remains sequestered within the cells despite adequate or even increased systemic iron stores and is thus unavailable for erythropoiesis. FID may be due to any number of causes, for example, chronic diseases, infection, inflammation, and / or malignant diseases. In some embodiments, functional iron deficiency is caused by blockage of iron mobilization from reticuloendothelial cells. In some embodiments, FID is caused by an increase of hepcidin level in the subject. In some embodiments, hepcidin prevents the delivery of iron to blood plasma from intestinal cells absorbing iron, from erythrocyte- recycling macrophages, and from iron-storing hepatocytes. In some embodiments, hepcidin inhibits iron transport by binding to the iron export channel ferroportin which is located on the basolateral surface of gut enterocytes and the plasma membrane of reticuloendothelial cells (macrophages). In some embodiments, inhibiting ferroportin prevents iron from being exported and the iron is sequestered in the cells. In some embodiments, by inhibiting ferroportin, hepcidin prevents enterocytes from allowing iron into the hepatic portal system, thereby reducing dietary iron absorption. In some embodiments, a subject having MDS (e.g., any MDS categories described herein) that is functional iron deficient has high hepcidin levels relative to a subject that does not have MDS, or a subject that has MDS without being functionally iron deficient. [000158] In some embodiments, FID manifests with a set of hematological parameters that distinguishes from true iron deficiency, e.g., normal or high circulating ferritin levels (e.g., indicating normal or near normal iron storage), and reduced TSAT (e.g., indicating deficient iron availability). However, additional biomarkers (e.g., sTfR, sTfR / log ferrin, CHr) may also be predictive of functional iron deficiency. [000159] In some embodiments, a subject having MDS that is functionally iron deficient has a ferritin level within or above normal. Ferritin is a blood protein that contains iron, the level of which indicates how much iron the body stores. The normal range of ferritin is 24- 336 µg / L for man, and 11-307 µg / L for women. In some embodiments, a subject having MDS that is functionally iron deficient has a ferritin level of more than 100 µg / L (e.g., more than 100 µg / L, more than 110 µg / L, more than 120 µg / L, more than 130 µg / L, more than 140µg / L, more than 150 µg / L, more than 160 µg / L, more than 170 µg / L, more than 180 µg / L, more than 190 µg / L, more than 200 µg / L, more than 210 µg / L, more than 220 µg / L, more than 230 µg / L, more than 240 µg / L, more than 250 µg / L, more than 260 µg / L, more than 270 µg / L, more than 280 µg / L, more than 290 µg / L, more than 300 µg / L, more than 350 µg / L, more than 400 µg / L, more than 450 µg / L, more than 500 µg / L, or more). In some embodiments, a subject having MDS that is functionally iron deficient has a ferritin level in the range of 100-299 µg / L (e.g., 100-299 µg / L, 100-295 µg / L, 100-290 µg / L, 100-280 µg / L, 100-270 µg / L, 100-260 µg / L, 100-250 µg / L, 100-240 µg / L, 100-230 µg / L, 100-220 µg / L, 100-210 µg / L, 100-200 µg / L, 100-190 µg / L, 100-180 µg / L, 100-170 µg / L, 100-160 µg / L, 100-150 µg / L, 100-140 µg / L, 100-130 µg / L, 100-120 µg / L, 100-110 µg / L, 110-299 µg / L, 110-295 µg / L, 110-290 µg / L, 110-280 µg / L, 110-270 µg / L, 110-260 µg / L, 110-250 µg / L, 110-240 µg / L, 110-230 µg / L, 110-220 µg / L, 110-210 µg / L, 110-200 µg / L, 110-190 µg / L, 110-180 µg / L, 110-170 µg / L, 110-160 µg / L, 110-150 µg / L, 110-140 µg / L, 110-130 µg / L, 110-120 µg / L, 120-299 µg / L, 120-295 µg / L, 120-290 µg / L, 120-280 µg / L, 120-270 µg / L, 120-260 µg / L, 120-250 µg / L, 120-240 µg / L, 120-230 µg / L, 120-220 µg / L, 120-210 µg / L, 120-200 µg / L, 120-190 µg / L, 120-180 µg / L, 120-170 µg / L, 120-160 µg / L, 120-150 µg / L, 120-140 µg / L, 120-130 µg / L, 150-299 µg / L, 150-295 µg / L, 150-290 µg / L, 150-280 µg / L, 150-270 µg / L, 150-260 µg / L, 150-250 µg / L, 150-240 µg / L, 150-230 µg / L, 150-220 µg / L, 150-210 µg / L, 150-200 µg / L, 150-190 µg / L, 150-180 µg / L, 150-170 µg / L, 150-160 µg / L, 180-299 µg / L, 180-295 µg / L, 180-290 µg / L, 180-280 µg / L, 180-270 µg / L, 180-260 µg / L, 180-250 µg / L, 180-240 µg / L, 180-230 µg / L, 180-220 µg / L, 180-210 µg / L, 180-200 µg / L, 180-190 µg / L, 200-299 µg / L, 200-295 µg / L, 200-290 µg / L, 200-280 µg / L, 200-270 µg / L, 200-260 µg / L, 200-250 µg / L, 200-240 µg / L, 200-230 µg / L, 200-220 µg / L, 200-210 µg / L, 220-299 µg / L, 220-295 µg / L, 220-290 µg / L, 220-280 µg / L, 220-270 µg / L, 220-260 µg / L, 220-250 µg / L, 220-240 µg / L, 220-230 µg / L, 250-299 µg / L, 250-295 µg / L, 250-290 µg / L, 250-280 µg / L, 250-270 µg / L, 250-260 µg / L, 280-299 µg / L, 280-295 µg / L, 280-290 µg / L). [000160] In some embodiments, a subject having MDS that is functionally iron deficient has a transferrin saturation level (TSAT%) level lower than normal. In some embodiments, a normal range of TSAT% is about 20%-50%. In some embodiments, a subject having MDS that is functionally iron deficient has a TSAT% level of less than 20% (e.g., less than 20%, less than 19%, less than 18%, less than 17%, less than 16%, less than 15%, less than 14%, less than 13%, less than 12%, less than 11%, less than 10%, less than 9%, less than 8%, lessthan 7%, less than 6%, less than 5%, less than 4%, less than 3%, less than 2%, or less than 1%). In some embodiments, a subject having MDS that is functionally iron deficient has a TSAT% level in the range of 1% to 20% (e.g., 1% to 20%, 1% to 19%, 1% to 18%, 1% to 17%, 1% to 16%, 1% to 15%, 1% to 14%, 1% to 13%, 1% to 12%, 1% to 11%, 1% to 10%, 1% to 9%, 1% to 8%, 1% to 7%, 1% to 6%, 1% to 5%, 1% to 4%, 1% to 3%, 1% to 2%, 3% to 20%, 3% to 19%, 3% to 18%, 3% to 17%, 3% to 16%, 3% to 15%, 3% to 14%, 3% to 13%, 3% to 12%, 3% to 11%, 3% to 10%, 3% to 9%, 3% to 8%, 3% to 7%, 3% to 6%, 3% to 5%, 3% to 4%, 5% to 20%, 5% to 19%, 5% to 18%, 5% to 17%, 5% to 16%, 5% to 15%, 5% to 14%, 5% to 13%, 5% to 12%, 5% to 11%, 5% to 10%, 5% to 9%, 5% to 8%, 5% to 7%, 5% to 6%, 8% to 20%, 8% to 19%, 8% to 18%, 8% to 17%, 8% to 16%, 8% to 15%, 8% to 14%, 8% to 13%, 8% to 12%, 8% to 11%, 8% to 10%, 8% to 9%, 10% to 20%, 10% to 19%, 10% to 18%, 10% to 17%, 10% to 16%, 10% to 15%, 10% to 14%, 10% to 13%, 10% to 12%, 10% to 11%, 12% to 20%, 12% to 19%, 12% to 18%, 12% to 17%, 12% to 16%, 12% to 15%, 12% to 14%, 12% to 13%, 15% to 20%, 15% to 19%, 15% to 18%, 15% to 17%, 15% to 16%, 18% to 20%, 18% to 19%, or 19% to 20%. [000161] In some embodiments, a subject having MDS has an elevated circulating hepcidin level (e.g., relative to a healthy subject of similar age and gender). In some embodiments, a subject having MDS that has functional iron deficiency has an elevated circulating hepcidin level (e.g., relative to a healthy subject of similar age and gender, or a subject having MDS without being functionally iron deficient). In some embodiments, a normal range of hepcidin is 1-55 ng / ml. In some embodiments, a subject having MDS that is functionally iron deficient has a hepcidin level of more than 55 ng / ml (e.g., more than 55 ng / ml, more than 55 ng / ml, more than 60 ng / ml, more than 65 ng / ml, more than 70 ng / ml, more than 75 ng / ml, more than 80 ng / ml, more than 85 ng / ml, more than 90 ng / ml, more than 95 ng / ml, more than 100 ng / ml, more than 150 ng / ml, more than 200 ng / ml, more than 250 ng / ml, more than 300 ng / ml, more than 350 ng / ml, more than 400 ng / ml, more than 450 ng / ml, or more than 500 ng / ml). In some embodiments, a subject having MDS that is functionally iron deficient has an elevated circulating hepcidin level by at least 5%, (e.g., at least 5%, at least 10%, at least 15%, at least 20%, at least 25%, at least 30%, at least 35%, at least 40%, at least 45%, at least 50%, at least 55%, at least 60%, at least 65%, at least 70%, at least 75%, at least 80%, at least 85%, at least 90%, at least 95%, at least 100%, at least 1.5 times, at least 2 times, at least 3 times, at least 4 times, at least 5 times, at least 10 times, at least 20 times, at least 50 times or at least 100 times) relative to a subject not having MDS, or a subject having MDS without being functionally iron deficient).[000162] In some embodiments, a subject having MDS (e.g., a MDS subject that is functionally iron deficient) has anemia. As used herein, the term “anemia” refers to a cytopenia in which erythrocytes are reduced relative to normal. Anemia may be due to any of a number of causes, for example, iron deficiency, vitamin deficiency, chronic disease (e.g., bone marrow disease, sickle cell anemia), aplastic anemia, hemolytic anemia, and thalassemia. Anemia may be macrocytic (i.e., with presence of abnormally large red blood cells), microcytic (i.e., with presence of abnormally small red blood cells), or normocytic (i.e., with presence of normal sized red blood cells). In some embodiments, a subject having MDS develops anemia due to functional iron deficiency. Symptoms of anemia often include fatigue, weakness, shortness of breath, pale skin, and dizziness. Anemia is often a symptom of an underlying condition. Several methods of determining anemia exist, including determining a concentration of hemoglobin (Hb), hematocrit (Hct), or red blood cell (RBC) count in the peripheral blood. Normal Hb concentration varies across populations, but typically range from about 11.5g / dL to 13.7g / dL in adults. Normal hematocrit values are between 36-48% for women and 40-54% for men. Normal RBC counts are typically between 4.2-5.4 million cells / mcL for women and 4.7-6.1 million cells / mcL. Values below the identified reference values may be indicative of anemia. Treatments for anemia depend on the likely cause but are generally directed to increasing iron in the blood; these treatments typically include dietary supplements, blood transfusions, or bone marrow transplants. [000163] In some embodiments, a subject having or at risk of developing MDS has refractory anemia. As used herein, the term “refractory anemia” (RA) refers to a form of anemia which is non-responsive to typical treatments (e.g., dietary iron supplements). RA is typically associated with dyserythropoiesis, dysplasia, low percentage of blasts in both the peripheral blood and the bone marrow (<5%), and low presence or absence of ringed sideroblasts (<15%). RA is a common symptom to all MDS categories; indeed, previous (pre- 2016) WHO categorizations of MDS used the term RA and MDS synonymously. In some embodiments, a subject having MDS with anemia is not responsive to typical treatment for anemia due to being functionally iron deficient. In some embodiments, a subject having MDS with high circulating hepcidin has sufficient iron store but mobilization of cellular iron store is inhibited by elevated level of hepcidin. [000164] In some embodiments, a subject having MDS with anemia has a hemoglobin level of less than 10 g / dL (e.g., less than 10 g / dL, less than 9.8 g / dL, less than 9.5 g / dL, less than 9.3 g / dL, less than 9 g / dL, less than 8.8 g / dL, less than 8.5 g / dL, less than 8.3 g / dL, less than 8 g / dL, less than 7.8 g / dL, less than 7.5 g / dL, less than 7.2 g / dL, less than 6.8 g / dL, lessthan 6.5 g / dL, less than 6.2 g / dL, less than 6 g / dL, or less). In some embodiments, a subject having MDS with anemia has a hemoglobin level in the range of 6-10 g / dL (e.g., 6-10 g / dL, 6-9.8 g / dL, 6-9.5 g / dL, 6-9.2 g / dL, 6-9 g / dL, 6-8.8 g / dL, 6-8.5 g / dL, 6-8.2 g / dL, 6-8 g / dL, 6- 7.8 g / dL, 6-7.5 g / dL, 6-7.2 g / dL, 6-7 g / dL, 6-6.8 g / dL, 6-6.5 g / dL, 6-6.2 g / dL, 6.2-10 g / dL, 6.2-9.8 g / dL, 6.2-9.5 g / dL, 6.2-9.2 g / dL, 6.2-9 g / dL, 6.2-8.8 g / dL, 6.2-8.5 g / dL, 6.2-8.2 g / dL, 6.2-8 g / dL, 6.2-7.8 g / dL, 6.2-7.5 g / dL, 6.2-7.2 g / dL, 6.2-7 g / dL, 6.2-6.8 g / dL, 6.2-6.5 g / dL, 6.5-10 g / dL, 6.5-9.8 g / dL, 6.5-9.5 g / dL, 6.5-9.2 g / dL, 6.5-9 g / dL, 6.5-8.8 g / dL, 6.5-8.5 g / dL, 6.5-8.2 g / dL, 6.5-8 g / dL, 6.5-7.8 g / dL, 6.5-7.5 g / dL, 6.5-7.2 g / dL, 6.5-7 g / dL, 6.5-6.8 g / dL, 6.8-10 g / dL, 6.8-9.8 g / dL, 6.8-9.5 g / dL, 6.8-9.2 g / dL, 6.8-9 g / dL, 6.8-8.8 g / dL, 6.8-8.5 g / dL, 6.8-8.2 g / dL, 6.8-8 g / dL, 6.8-7.8 g / dL, 6.8-7.5 g / dL, 6.8-7.2 g / dL, 6.8-7 g / dL, 7-10 g / dL, 7- 9.8 g / dL, 7-9.5 g / dL, 7-9.2 g / dL, 7-9 g / dL, 7-8.8 g / dL, 7-8.5 g / dL, 7-8.2 g / dL, 7-8 g / dL, 7-7.8 g / dL, 7-7.5 g / dL, 7-7.2 g / dL, 7.2-10 g / dL, 7.2-9.8 g / dL, 7.2-9.5 g / dL, 7.2-9.2 g / dL, 7.2-9 g / dL, 7.2-8.8 g / dL, 7.2-8.5 g / dL, 7.2-8.2 g / dL, 7.2-8 g / dL, 7.2-7.8 g / dL, 7.2-7.5 g / dL, 7.5-10 g / dL, 7.5-9.8 g / dL, 7.5-9.5 g / dL, 7.5-9.2 g / dL, 7.5-9 g / dL, 7.5-8.8 g / dL, 7.5-8.5 g / dL, 7.5-8.2 g / dL, 7.5-8 g / dL, 7.5-7.8 g / dL, 7.8-10 g / dL, 7.8-9.8 g / dL, 7.8-9.5 g / dL, 7.8-9.2 g / dL, 7.8-9 g / dL, 7.8-8.8 g / dL, 7.8-8.5 g / dL, 7.8-8.2 g / dL, 7.8-8 g / dL, 8-10 g / dL, 8-9.8 g / dL, 8-9.5 g / dL, 8-9.2 g / dL, 8-9 g / dL, 8-8.8 g / dL, 8-8.5 g / dL, 8-8.2 g / dL, 8.2-10 g / dL, 8.2-9.8 g / dL, 8.2-9.5 g / dL, 8.2-9.2 g / dL, 8.2-9 g / dL, 8.2-8.8 g / dL, 8.2-8.5 g / dL, 8.5-10 g / dL, 8.5-9.8 g / dL, 8.5-9.5 g / dL, 8.5-9.2 g / dL, 8.5-9 g / dL, 8.5-8.8 g / dL, 8.8-10 g / dL, 8.8-9.8 g / dL, 8.8-9.5 g / dL, 8.8-9.2 g / dL, 8.8-9 g / dL, 9-10 g / dL, 9-9.8 g / dL, 9-9.5 g / dL, 9-9.2 g / dL, 9.2-10 g / dL, 9.2-9.8 g / dL, 9.2-9.5 g / dL, 9.5-10 g / dL, 9.5-9.8 g / dL, or 9.8-10 g / dL). [000165] In some embodiments, a subject having or at risk of developing MDS has hepatic iron content of less than 7 mg / g dry weight (e.g., less than 7 mg / g dry weight, less than 6 mg / g dry weight, less than 5 mg / g dry weight, less than 4 mg / g dry weight, less than 3 mg / g dry weight, less than 2 mg / g dry weight, or less than 1 mg / g dry weight). [000166] In some embodiments, a subject having or at risk of developing MDS has a cytopenia. As used herein, the term “cytopenia” refers to any reduction in the number of mature erythrocytes (i.e., red blood cells), leukocytes (i.e., white blood cells), and / or thrombocytes (i.e., platelets) in the body. Types of cytopenias include anemia (i.e., cytopenia of erythrocytes), leukopenia (i.e., cytopenia of leukocytes, for example, neutropenia), and thrombocytopenia (i.e., cytopenia of thrombocytes). Cytopenias can be detected via assays of the peripheral blood, for example, by count of a given cell type (e.g., complete blood cell count).[000167] In some embodiments, a subject having or at risk of developing MDS has a single cytopenia. In some embodiments, the single cytopenia is anemia. In some embodiments, the single cytopenia is leukopenia. In some embodiments, the single cytopenia is neutropenia. In some embodiments, the single cytopenia is thrombocytopenia. In some embodiments, a subject having or at risk of developing MDS has one or more cytopenias. In some embodiments, a subject having or at risk of developing MDS has two or more cytopenias. In some embodiments, a subject having or at risk of developing MDS has two cytopenias (i.e., bicytopenia). In some embodiments, the two cytopenias are anemia and leukopenia. In some embodiments, the two cytopenias are anemia and thrombocytopenia. In some embodiments, the two cytopenias are leukopenia and thrombocytopenia. In some embodiments, a subject having or at risk of developing MDS has three cytopenias (i.e., panocytopenia). In some embodiments, a subject having MDS has anemia but does not have leukopenia (e.g., neutropenia). In some embodiments, a subject having MDS has anemia but does not have thrombocytopenia. In some embodiments, a subject having MDS has anemia but does not have leukopenia (e.g., neutropenia) or thrombocytopenia. [000168] In some embodiments, a subject having MDS with anemia has red blood cell count in the range of 2x1012to 8x1012cells / L, 2x1012to 7x1012cells / L, 2x1012to 6x1012cells / L, 2x1012to 5x1012cells / L, 2x1012to 4x1012cells / L, 2x1012to 3x1012cells / L, 3x1012to 8x1012cells / L, 3x1012to 7x1012cells / L, 3x1012to 6x1012cells / L, 3x1012to 5x1012cells / L, 3x1012to 4x1012cells / L, 4x1012to 8x1012cells / L, 4x1012to 7x1012cells / L, 4x1012to 6x1012cells / L, 4x1012to 5x1012cells / L, 5x1012to 8x1012cells / L, 5x1012to 7x1012cells / L, 5x1012to 6x1012cells / L, 6x1012to 8x1012cells / L, or 7x1012to 8x1012cells / L. [000169] In some embodiments, a subject having MDS with leukopenia has a total white blood cell count of less than 5x104 / µl (e.g., less than 5x104 / µl, less than 4.5x104 / µl, less than 4x104 / µl, less than 3.5x104 / µl, less than 3x104 / µl, less than 2.5x104 / µl, less than 2x104 / µl, less than 1.5x104 / µl, less than 1x104 / µl, or less). In some embodiments, a subject having MDS with cytopenia has a total white blood cell count in the range of 1x104to 5x104 / µl (e.g., 1x104to 5x104 / µl, 1x104to 4.5x104 / µl, 1x104to 4x104 / µl, 1x104to 3.5x104 / µl, 1x104to 3x104 / µl, 1x104to 2.5x104 / µl, 1x104to 2x104 / µl, 1x104to 1.5x104 / µl, 1.5x104to 5x104 / µl, 1.5x104to 4.5x104 / µl, 1.5x104to 4x104 / µl, 1.5x104to 3.5x104 / µl, 1.5x104to 3x104 / µl, 1.5x104to 2.5x104 / µl, 1.5x104to 2x104 / µl, 2x104to 5x104 / µl, 2x104to 4.5x104 / µl, 2x104to 4x104 / µl, 2x104to 3.5x104 / µl, 2x104to 3x104 / µl, 2x104to 2.5x104 / µl, 2.5x104to 5x104 / µl, 2.5x104to 4.5x104 / µl, 2.5x104to 4x104 / µl, 2.5x104to 3.5x104 / µl, 2.5x104to3x104 / µl, 3x104to 5x104 / µl, 3x104to 4.5x104 / µl, 3x104to 4x104 / µl, 3x104to 3.5x104 / µl, 3.5x104to 5x104 / µl, 3.5x104to 4.5x104 / µl, 3.5x104to 4x104 / µl, 4x104to 5x104 / µl, 4x104to 4.5x104 / µl, or 4.5x104to 5x104 / µl). [000170] In some embodiments, a subject having MDS with thrombocytopenia has a total platelet count in the range of 2.5x104to 1x106 / µL (e.g., 2.5x104to 9x105 / µL, 2.5x104to 8x105 / µL, 2.5x104to 7x105 / µL, 2.5x104to 6x105 / µL, 2.5x104to 5x105 / µL, 2.5x104to 4x105 / µL, 2.5x104to 3x105 / µL, 2.5x104to 2x105 / µL, 2.5x104to 1x105 / µL, 2.5x104to 9x104 / µL, 2.5x104to 8x104 / µL, 2.5x104to 7x104 / µL, 2.5x104to 6x104 / µL, 2.5x104to 5x104 / µL, 2.5x104to 4x104 / µL, 2.5x104to 3x104 / µL, 3x104to 9x105 / µL, 3x104to 8x105 / µL, 3x104to 7x105 / µL, 3x104to 6x105 / µL, 3x104to 5x105 / µL, 3x104to 4x105 / µL, 3x104to 3x105 / µL, 3x104to 2x105 / µL, 3x104to 1x105 / µL, 3x104to 9x104 / µL, 3x104to 8x104 / µL, 3x104to 7x104 / µL, 3x104to 6x104 / µL, 3x104to 5x104 / µL, 3x104to 4x104 / µL, 4x104to 9x105 / µL, 4x104to 8x105 / µL, 4x104to 7x105 / µL, 4x104to 6x105 / µL, 4x104to 5x105 / µL, 4x104to 4x105 / µL, 4x104to 3x105 / µL, 4x104to 2x105 / µL, 4x104to 1x105 / µL, 4x104to 9x104 / µL, 4x104to 8x104 / µL, 4x104to 7x104 / µL, 4x104to 6x104 / µL, 4x104to 5x104 / µL, 5x104to 9x105 / µL, 5x104to 8x105 / µL, 5x104to 7x105 / µL, 5x104to 6x105 / µL, 5x104to 5x105 / µL, 5x104to 4x105 / µL, 5x104to 3x105 / µL, 5x104to 2x105 / µL, 5x104to 1x105 / µL, 5x104to 9x104 / µL, 5x104to 8x104 / µL, 5x104to 7x104 / µL, 5x104to 6x104 / µL, 6x104to 9x105 / µL, 6x104to 8x105 / µL, 6x104to 7x105 / µL, 6x104to 6x105 / µL, 6x104to 5x105 / µL, 6x104to 4x105 / µL, 6x104to 3x105 / µL, 6x104to 2x105 / µL, 6x104to 1x105 / µL, 6x104to 9x104 / µL, 6x104to 8x104 / µL, 6x104to 7x104 / µL, 7x104to 9x105 / µL, 7x104to 8x105 / µL, 7x104to 7x105 / µL, 7x104to 6x105 / µL, 7x104to 5x105 / µL, 7x104to 4x105 / µL, 7x104to 3x105 / µL, 7x104to 2x105 / µL, 7x104to 1x105 / µL, 7x104to 9x104 / µL, 7x104to 8x104 / µL, 8x104to 9x105 / µL, 8x104to 8x105 / µL, 8x104to 7x105 / µL, 8x104to 6x105 / µL, 8x104to 5x105 / µL, 8x104to 4x105 / µL, 8x104to 3x105 / µL, 8x104to 2x105 / µL, 8x104to 1x105 / µL, 8x104to 9x104 / µL, 9x104to 9x105 / µL, 9x104to 8x105 / µL, 9x104to 7x105 / µL, 9x104to 6x105 / µL, 9x104to 5x105 / µL, 9x104to 4x105 / µL, 9x104to 3x105 / µL, 9x104to 2x105 / µL, 9x104to 1x105 / µL, 1x105to 9x105 / µL, 1x105to 8x105 / µL, 1x105to 7x105 / µL, 1x105to 6x105 / µL, 1x105to 5x105 / µL, 1x105to 4x105 / µL, 1x105to 3x105 / µL, 1x105to 2x105 / µL, 2x105to 9x105 / µL, 2x105to 8x105 / µL, 2x105to 7x105 / µL, 2x105to 6x105 / µL, 2x105to 5x105 / µL, 2x105to 4x105 / µL, 2x105to 3x105 / µL, 3x105to 9x105 / µL, 3x105to 8x105 / µL, 3x105to 7x105 / µL, 3x105to 6x105 / µL, 3x105to 5x105 / µL, 3x105to 4x105 / µL, 4x105to 9x105 / µL, 4x105to 8x105 / µL, 4x105to 7x105 / µL, 4x105to 6x105 / µL, 4x105to 5x105 / µL,5x105to 9x105 / µL, 5x105to 8x105 / µL, 5x105to 7x105 / µL, 5x105to 6x105 / µL, 6x105to 9x105 / µL, 6x105to 8x105 / µL, 6x105to 7x105 / µL, 7x105to 9x105 / µL, 7x105to 8x105 / µL, or 8x105to 9x105 / µL). [000171] In some embodiments, a subject having MDS does not have liver damage. In some embodiments, a subject having MDS has an aspartate aminotransferase (AST) level of less than 3.0x upper limit of normal (ULN) (e.g., less than 3.0x ULN, less than 2.5x ULN, less than 2x ULN, less than 1.5x ULN, less than 1.0x ULN, less than 0.5x ULN, or less than 0.2x ULN). In some embodiments, a subject having MDS has an alanine transaminase (ALT) level of less than 3.0x upper limit of normal (ULN) (e.g., less than 3.0x ULN, less than 2.5x ULN, less than 2x ULN, less than 1.5x ULN, less than 1.0x ULN, less than 0.5x ULN, or less than 0.2x ULN). In some embodiments, a subject having MDS has a direct bilirubin level of less than 2.0x upper limit of normal (ULN) (e.g., less than 2x ULN, less than 1.8x ULN, less than 1.5x ULN, less than 1.2x ULN, less than 1.0x ULN, less than 0.8x ULN, less than 0.5x ULN, or less than 0.2x ULN). [000172] In some embodiments, a subject having MDS has an estimated glomerular filtration rate (eGFR) level of at least 30 mL / min / 1.73m2(e.g., at least 35 mL / min / 1.73m2, at least 40 mL / min / 1.73m2, at least 45 mL / min / 1.73m2, at least 50 mL / min / 1.73m2, at least 55 mL / min / 1.73m2, at least 60 mL / min / 1.73m2, at least 65 mL / min / 1.73m2, at least 70 mL / min / 1.73m2, at least 75 mL / min / 1.73m2, at least 80 mL / min / 1.73m2, at least 85 mL / min / 1.73m2, at least 90 mL / min / 1.73m2, or more). [000173] In some embodiments, a subject having MDS have previously received treatments for treating MDS, and / or cytopenia (e.g., anemia, leukopenia, and / or thrombocytopenia) associated with MDS, such as transfusions (e.g., RBC transfusion and / or platelet transfusion), erythropoiesis stimulating agents (e.g., EPO), lenalidomide, androgens, erythropoietin, luspatercept, sotatercept, Granulocyte colony-stimulating factor (G-CSF), Granulocyte-macrophage colony-stimulating factor (GM-CSF), or corticosteroid. [000174] In some embodiments, a subject having MDS does not have Hereditary hemochromatosis. In some embodiments, a subject having MDS does not have hemoglobinopathy or intrinsic RBC defect associated with anemia (e.g., sickle cell disease anemia). In some embodiments, a subject having MDS did not undergo splenectomy. In some embodiments, a subject does not have active immune-mediated hemolytic anemia. In some embodiments, a subject does not have bleeding (e.g., surgery or bleeding disorder) that decreases hemoglobin of more than ≥2 g / dL. In some embodiments, a subject does not have bleeding (e.g., surgery or bleeding disorder) that require transfusion. In some embodiments, asubject has not received a hematopoietic cell transplant within 10 years of the administration of the anti-HJV antibody. In some embodiments, a subject has not received iron chelation therapy within 28 days of the administration of the anti-HJV antibody. In some embodiments, a subject does not have secondary MDS (e.g., MDS arising from chemical injury or treatment with chemotherapy and / or radiation for other diseases. [000175] In some embodiments, the present disclosure provides a method of administering an anti-HJV antibody described herein to a subject having MDS. In some embodiments, the present disclosure provides method of administering an anti-HJV antibody described herein to a functionally iron deficient subject having MDS. In some embodiments, the present disclosure provides method of administering an anti-HJV antibody described herein to a subject having MDS with elevated hepcidin level. In some embodiments, the administration results in release of cellular iron stores (i.e., mobilization of iron from cellular iron store from liver, spleen, and / or bone marrow such that the iron is available for erythropoiesis). In some embodiments, the administration results in release of cellular iron stores in the amount sufficient to treat anemia in the subject. In some embodiments, release of cellular iron store is determined by evaluating serum iron, TSAT%, red blood cell count, hemoglobin, Total iron binding capacity (TIBC), and / or hepcidin. Each of these parameters can be measured using suitable methods. [000176] In some embodiments, the administration of an anti-HJV antibody increases hemoglobin level in the subject by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between80% and 90%, or between 90% and 100% relative to hemoglobin level in the subject before the administration. In some embodiments, the administration of an anti-HJV antibody increases hemoglobin level in the subject by at least 1-fold, at least 1.5 folds, at least 2 folds, at least 3 folds or more relative to the hemoglobin level before the administration. In some embodiments, the administration of an anti-HJV antibody described herein increases hemoglobin level at least 1 g / dL (e.g., at least 1 g / dL, at least 1.1 g / dL, at least 1.2 g / dL, at least 1.3 g / dL, at least 1.4 g / dL, at least 1.5 g / dL, at least 1.6 g / dL, at least 1.7 g / dL, at least 1.8 g / dL, at least 1.9 g / dL, at least 2 g / dL, at least 2.1 g / dL, at least 2.2 g / dL, at least 2.3 g / dL, at least 2.4 g / dL, at least 2.5 g / dL, at least 2.6 g / dL, at least 2.7 g / dL, at least 2.8 g / dL, at least 2.9 g / dL, at least 3 g / dL, at least 3.1 g / dL, at least 3.2 g / dL, at least 3.3 g / dL, at least 3.4 g / dL, at least 3.5 g / dL, at least 3.6 g / dL, at least 3.7 g / dL, at least 3.8 g / dL, at least 3.9 g / dL, at least 4 g / dL, at least 4.1 g / dL, at least 4.2 g / dL, at least 4.3 g / dL, at least 4.4 g / dL, at least 4.5 g / dL, at least 4.6 g / dL, at least 4.7 g / dL, at least 4.8 g / dL, at least 4.9 g / dL, at least 5 g / dL, or more). In some embodiments, the administration of an anti-HJV antibody described herein increases hemoglobin level by the range of 1-5 g / dL (e.g., 1-5 g / dL, 1-4.8 g / dL, 1-4.5 g / dL, 1-4.2 g / dL, 1-4 g / dL, 1-3.8 g / dL, 1-3.5 g / dL, 1-3.2 g / dL, 1-3 g / dL, 1-2.8 g / dL, 1-2.5 g / dL, 1- 2.2 g / dL, 1-2 g / dL, 1-1.8 g / dL, 1-1.5 g / dL, 1-1.2 g / dL, 1.5-5 g / dL, 1.5-4.8 g / dL, 1.5-4.5 g / dL, 1.5-4.2 g / dL, 1.5-4 g / dL, 1.5-3.8 g / dL, 1.5-3.5 g / dL, 1.5-3.2 g / dL, 1.5-3 g / dL, 1.5-2.8 g / dL, 1.5-2.5 g / dL, 1.5-2.2 g / dL, 1.5-2 g / dL, 1.5-1.8 g / dL, 1.8-5 g / dL, 1.8-4.8 g / dL, 1.8-4.5 g / dL, 1.8-4.2 g / dL, 1.8-4 g / dL, 1.8-3.8 g / dL, 1.8-3.5 g / dL, 1.8-3.2 g / dL, 1.8-3 g / dL, 1.8-2.8 g / dL, 1.8-2.5 g / dL, 1.8-2.2 g / dL, 1.8-2 g / dL, 2-5 g / dL, 2-4.8 g / dL, 2-4.5 g / dL, 2-4.2 g / dL, 2-4 g / dL, 2-3.8 g / dL, 2-3.5 g / dL, 2-3.2 g / dL, 2-3 g / dL, 2-2.8 g / dL, 2-2.5 g / dL, 2-2.2 g / dL, 2.2-5 g / dL, 2.2-4.8 g / dL, 2.2-4.5 g / dL, 2.2-4.2 g / dL, 2.2-4 g / dL, 2.2-3.8 g / dL, 2.2-3.5 g / dL, 2.2-3.2 g / dL, 2.2-3 g / dL, 2.2-2.8 g / dL, 2.2-2.5 g / dL, 2.5-5 g / dL, 2.5-4.8 g / dL, 2.5-4.5 g / dL, 2.5-4.2 g / dL, 2.5-4 g / dL, 2.5-3.8 g / dL, 2.5-3.5 g / dL, 2.5-3.2 g / dL, 2.5-3 g / dL, 2.5-2.8 g / dL, 2.8-5 g / dL, 2.8-4.8 g / dL, 2.8-4.5 g / dL, 2.8-4.2 g / dL, 2.8-4 g / dL, 2.8-3.8 g / dL, 2.8-3.5 g / dL, 2.8-3.2 g / dL, 2.8-3 g / dL, 3-5 g / dL, 3-4.8 g / dL, 3-4.5 g / dL, 3-4.2 g / dL, 3-4 g / dL, 3-3.8 g / dL, 3-3.5 g / dL, 3- 3.2 g / dL, 3.2-5 g / dL, 3.2-4.8 g / dL, 3.2-4.5 g / dL, 3.2-4.2 g / dL, 3.2-4 g / dL, 3.2-3.8 g / dL, 3.2- 3.5 g / dL, 3.5-5 g / dL, 3.5-4.8 g / dL, 3.5-4.5 g / dL, 3.5-4.2 g / dL, 3.5-4 g / dL, 3.5-3.8 g / dL, 3.8-5 g / dL, 3.8-4.8 g / dL, 3.8-4.5 g / dL, 3.8-4.2 g / dL, 3.8-4 g / dL, 4-5 g / dL, 4-4.8 g / dL, 4-4.5 g / dL, 4-4.2 g / dL, 4.2-5 g / dL, 4.2-4.8 g / dL, 4.2-4.5 g / dL, 4.5-5 g / dL, 4.5-4.8 g / dL, 4.8-5 g / dL. [000177] In some embodiments, the administration of an anti-HJV antibody described herein increases RBC count in the subject by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%,between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, between 90% and 100%, 1-50 folds, 1-45 folds, 1-40 folds, 1-35 folds, 1-30 folds, 1-25 folds, 1-20 folds, 1-15 folds, 1-10 folds, 1-9 folds, 1-8 folds, 1-7 folds, 1-6 folds, 1-5 folds, 1-4 folds, 1-3 folds, 1-2 folds, 5-50 folds, 5-45 folds, 5-40 folds, 5-35 folds, 5-30 folds, 5-25 folds, 5-20 folds, 5-15 folds, 5-10 folds, 5-9 folds, 5-8 folds, 5-7 folds, 5-6 folds, 10-15 folds, 10-20 folds, 10-30 folds, 10-40 folds, 10-50 folds, 20-30 folds, 20-40 folds, 20-50 folds, 30-40 folds, 30-50 folds, or 40-50 folds) relative to the RBC count prior to administration. [000178] In some embodiments, the administration of an anti-HJV antibody described herein increases TSAT% in the subject by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, between 90% and 100%, 1-50 folds, 1-45 folds, 1-40 folds, 1-35 folds, 1-30 folds, 1-25 folds, 1-20 folds, 1-15 folds, 1-10 folds, 1-9 folds, 1-8 folds, 1-7 folds, 1-6 folds, 1-5 folds, 1-4 folds, 1-3 folds, 1-2 folds, 5-50 folds, 5-45 folds, 5-40 folds, 5-35 folds, 5-30 folds, 5-25 folds, 5-20 folds, 5-15 folds, 5-10 folds, 5-9 folds, 5-8 folds, 5-7 folds, 5-6 folds, 10-15 folds, 10-20 folds, 10-30 folds, 10-40 folds, 10-50 folds, 20-30 folds, 20-40 folds, 20- 50 folds, 30-40 folds, 30-50 folds, or 40-50 folds) relative to the TSAT% prior to administration. [000179] In some embodiments, the administration of an anti-HJV antibody described herein decreases circulating hepcidin level in the subject by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, between 90% and 100%) relative to the circulating hepcidin level prior to administration. [000180] In some embodiments, the administration of an anti-HJV antibody described herein increases total iron binding capacity (TIBC) in the subject by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, between 90% and 100%, 1-50 folds, 1-45 folds, 1-40 folds, 1-35 folds, 1-30 folds, 1-25 folds, 1-20 folds, 1-15 folds, 1-10 folds, 1-9 folds, 1-8 folds, 1-7 folds, 1-6 folds, 1-5 folds, 1-4 folds, 1-3 folds, 1-2 folds, 5-50 folds, 5-45 folds, 5-40 folds, 5-35 folds, 5-30 folds, 5-25 folds, 5-20 folds, 5-15 folds, 5-10 folds, 5-9 folds, 5-8 folds, 5-7 folds, 5-6 folds, 10-15 folds, 10-20 folds, 10-30 folds, 10-40 folds, 10-50 folds, 20-30 folds, 20-40 folds, 20-50 folds, 30-40 folds, 30-50 folds, or 40-50 folds) relative to the TIBC prior to administration. [000181] In some embodiments, the administration of an anti-HJV antibody described herein increases the subject’s serum iron level by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, or between 90% and 100% compared to before administration. In some embodiments, after administration of an anti-HJV antibody, the subject’s serum ironlevel increases by more than 100% (e.g., at least 2-fold, at least 3-fold, at least 5-fold, at least 10-fold, at least 20-fold, at least 50-fold, at least 100-fold, at least 500-fold, at least 1000- fold, or more) compared to before administration. [000182] In some embodiments, the administration of an anti-HJV antibody described herein increases the subject’s mean corpuscular hemoglobin (MCH) by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%, between 30% and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, or between 90% and 100% compared to before administration. In some embodiments, after administration of an anti-HJV antibody, the subject’s MCH increases by more than 100% (e.g., at least 2-fold, at least 3-fold, at least 5-fold, at least 10-fold, at least 20-fold, at least 50-fold, at least 100-fold, at least 500-fold, at least 1000-fold, or more) compared to before administration. [000183] In some embodiments, the administration of an anti-HJV antibody described herein increases the subject’s mean corpuscular hemoglobin concentration (MCHC) by between 1% and 100%, between 5% and 100%, between 5% and 90%, between 5% and 80%, between 5% and 70%, between 5% and 60%, between 5% and 50%, between 5% and 40%, between 5% and 30%, between 5% and 20%, between 5% and 15%, between 10% and 100%, between 10% and 90%, between 10% and 80%, between 10% and 70%, between 10% and 60%, between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, between 10% and 15%, between 20% and 100%, between 20% and 90%, between 20% and 80%, between 20% and 70%, between 20% and 60%, between 20% and 50%, between 20% and 40%, between 20% and 30%, between 30% and 100%, between 30% and 90%,between 30% and 80%, between 30% and 70%, between 30% and 60%, between 30% and 50%, between 30% and 40%, between 40% and 100%, between 40% and 90%, between 40% and 80%, between 40% and 70%, between 40% and 60%, between 40% and 50%, between 50% and 100%, between 50% and 90%, between 50% and 80%, between 50% and 70%, between 50% and 60%, between 60% and 100%, between 60% and 90%, between 60% and 80%, between 60% and 70%, between 70% and 100%, between 70% and 90%, between 70% and 80%, between 80% and 100%, between 80% and 90%, or between 90% and 100% compared to before administration. In some embodiments, after administration of an anti- HJV antibody, the subject’s MCHC increases by more than 100% (e.g., at least 2-fold, at least 3-fold, at least 5-fold, at least 10-fold, at least 20-fold, at least 50-fold, at least 100-fold, at least 500-fold, at least 1000-fold, or more) compared to before administration. [000184] In some embodiments, an anti-HJV antibody described herein can be administered to the subject in combination with any suitable therapies for treating MDS and / or any conditions associated with MDS (e.g., cytopenia). In some embodiments, a subject having MDS has previously received therapies including transfusion, iron chelation, growth factor (e.g., GMSF, GMCSF), luspatercept, lenalidomide, immune modulator (e.g., corticosteroids), allogeneic stem cell transplantation, and / or hypomethylating agent (HMA). In some embodiments, an anti-HJV antibody described herein is administered sequentially with any of the other therapeutic agents for treating MDS and / or any conditions associated with MDS (e.g., cytopenia). In some embodiments, an anti-HJV antibody described herein is administered concurrently with any of the other therapeutic agents for treating MDS and / or any conditions associated with MDS (e.g., cytopenia). III. Hemojuvelin (HJV) Antagonists [000185] In some aspects, hemojuvelin antagonists are provided herein for reducing expression and / or function of hepcidin, e.g., for treating MDS in a functionally iron deficient subject having MDS. Generally, “hemojuvelin antagonist,” refers to a molecule that reduces expression of hemojuvelin or inhibits hemojuvelin activity, e.g., by binding to hemojuvelin. In some embodiments, the hemojuvelin antagonist is an antisense oligonucleotide (see, e.g., U.S. Patent No. 7,534,764; U.S. Patent Publication No. US 2014 / 127325; and International Publication No. WO 2016 / 180784, which are incorporated herein by reference). In some embodiments, the hemojuvelin antagonist is an antibody (e.g., an anti-HJV antibody described herein, or an anti-HJV antibody described in WO2020086736, which is incorporated herein by reference). In other embodiments, the hemojuvelin antagonist is asmall molecule compound that inhibits hemojuvelin, e.g., by competitive binding and / or chemical modification of hemojuvelin. In some embodiments, the hemojuvelin antagonist is a HJV fragment (see., e.g., an HJV fragment described by US Patent 8,507,435, which is incorporated herein by reference), or an HJV fusion protein (e.g., an HJV-Fc fusion protein described by US Patent 8,637,023, which is incorporated herein by reference). [000186] In some embodiments, the methods provided herein are based on a recognition that increases in serum or tissue iron trigger transcriptional induction of hepcidin via the BMP- SMAD signaling pathway. Generally, “HJV-induced BMP signaling” refers to signaling through BMP receptors that is induced by Hemojuvelin (HJV), which is a membrane bound co-receptor for bone morphogenetic protein (BMP) signaling. As discussed in Xia Y, et al., Hemojuvelin regulates hepcidin expression via a selective subset of BMP ligands and receptors independently of neogenin, Blood. 2008 May 15; 111(10): 5195–5204, in hepatocytes, HJV-induced BMP signaling positively regulates hepcidin mRNA expression. In some embodiments, HJV binds to BMP2, BMP4, BMP5, or BMP6 to induce BMP signaling, e.g., to positively regulate hepcidin levels in hepatocytes. In some embodiments, cleavage of HJV by matriptase-2 reduces the amount of cell surface HJV available to participate in BMP signaling. In some embodiments, induction of BMP signaling by HJV is independent of neogenin. However, in some embodiments, neogenin facilitates induction of BMP signaling by HJV, as discussed in Zhao et al, Neogenin Facilitates the Induction of Hepcidin Expression by Hemojuvelin in the Liver, J Biol Chem. 2016 Jun 3; 291(23): 12322–12335. In some embodiments, BMP6 is responsible for iron-dependent activation of the Smad signaling. In some embodiments, BMP6 is secreted from liver sinusoidal endothelial cells and binds to a BMP receptor (BMPR) on hepatocytes and thereby activates the SMAD signaling cascade. In such embodiments, HJV serves as a co-receptor for such BMP6, e.g., to positively regulate hepcidin levels in hepatocytes. In some embodiments, BMPs transduce signals by binding to one or a combination of type I and II serine / threonine kinase receptors. BMP type II receptors include BMPRII, ActRIIA, and ActRIIB. BMP type I receptors include ALK3, ALK6, and ALK2. In some embodiments, upon ligand binding, constitutively active type II receptors phosphorylate type I receptors, and type I receptors then phosphorylate intracellular receptor-activated Smads (R-Smads), namely Smad 1, Smad 5 and / or Smad 8. In such embodiments, activated R-Smads complex with the common partner Smad4 and translocate to the nucleus to regulate gene transcription, e.g., induction of hepcidin expression. In some embodiments, HJV serves as a BMP co-receptor to positively regulate hepcidin levels. In certain cells, e.g., hepatocytes, HJV-induced BMP signaling positively regulates hepcidinmRNA expression. In such embodiments, HJV binds to BMP2, BMP4, BMP5, and / or BMP6 to mediate BMP signaling, e.g., to positively regulate hepcidin levels in hepatocytes. In some embodiments, BMPs transduce signals by binding to one or a combination of type I and II serine / threonine kinase receptors. In some embodiments, upon ligand binding, constitutively active type II receptors phosphorylate type I receptors, and type I receptors then phosphorylate intracellular receptor-activated Smads (R-Smads), namely Smad 1, Smad 5 and / or Smad 8. In such embodiments, activated R-Smads complex with the common partner Smad4 and translocate to the nucleus to regulate gene transcription, e.g., induction of hepcidin expression. [000187] In some embodiments, the hemojuvelin antagonist binds to one or more proteins of the repulsive guidance molecule (RGM) family, including RGMa, RGMb, and RGMc (HJV). In some embodiments, the hemojuvelin antagonist selectively binds hemojuvelin (RGMc) over RGMa and RGMb. In some embodiments, the hemojuvelin antagonist selectively binds hemojuvelin (RGMc) and RGMa over RGMb. [000188] In some embodiments, the hemojuvelin antagonist is an antisense oligonucleotide that reduces expression of hemojuvelin (see, e.g., US7534764, entitled “Competitive regulation of hepcidin mRNA by soluble and cell-associated hemojuvelin,” issued May 19, 2009; US2014127325, entitled “Competitive regulation of hepcidin mRNA by soluble and cell-associated hemojuvelin”, issued May 19, 2009; and WO2016180784, entitled “Improved treatments using oligonucleotides”, published November 17, 2016, which are incorporated herein by reference). In some embodiments, the hemojuvelin antagonist is a small molecule compound that inhibits hemojuvelin, e.g., by competitive binding and / or chemical modification of hemojuvelin. [000189] In some embodiments, the HJV antagonist is a soluble HJV. In some embodiments, the soluble HJV is a soluble HJV-Fc fusion protein. In some embodiments, the soluble HJV is a soluble HJV as disclosed in US8318167B2, entitled “Methods and compositions for regulating iron homeostasis by modulation of BMP-6”. issued November 27, 2012; US9708379B2, entitled “COMPOSITIONS FOR REGULATING IRON HOMEOSTASIS AND METHODS OF USING SAME,” issued July 18, 2017, US10273273B2, entitled “COMPOSITIONS AND REGULATING IRON HOMEOSTASIS AND METHODS OF USING SAME,” issued April 30, 2019, US7968091B2, entitled “METHODS AND COMPOSITIONS TO REGULATE IRON METABOLISM,” issued June 28, 2011, US8637023B2, entitled “HEMOJUVELIN FUSION PROTEINS,” issued January 28, 2014, US8865168B2, entitled “METHODS AND COMPOSITIONS TO REGULATE HEPCIDINEXPRESSION,” issued October 21, 2014, US9556251B2, entitled “METHODS AND COMPOSITIONS TO REGULATE HEPCIDIN EXPRESSION,” issued January 31, 2017; US8895002B2, entitled “Hemojuvelin fusion proteins and uses thereof”, issued November 25, 2014; US7511018B2, entitled “Juvenile hemochromatosis gene (HFE2A) cleavage products and uses thereof”, issued March 31, 2009, the relevant contents of each of which are incorporated herein by reference. In some embodiments, the sHJV-Fc fusion protein is Ferruxmax. In some embodiments, the sHJV-Fc fusion protein is FMX-8. [000190] In some embodiments, the hemojuvelin antagonist is an antibody specific for hemojuvelin and / or one or more proteins of the RGM protein family (e.g., RGMa, RGMb). In some embodiments, the hemojuvelin antagonist is an antibody specific for RGMa. In some embodiments, the hemojuvelin antagonist is an antibody specific for hemojuvelin (RGMc) and / or RGMa, but not for RGMb. In some embodiments, antibodies specific for hemojuvelin and / or one or more RGM proteins is an anti-HJV antibody and / or one or more RGM proteins as disclosed in US10118958, entitled “Composition and method for the diagnosis and treatment of iron-related disorders”, issued November 6, 2018; US9636398, entitled “Composition and method for the diagnosis and treatment of iron-related disorders”, issued May 2, 2017; and US8507435, entitled “Juvenile hemochromatosis gene (HFE2A) cleavage products and uses thereof”, issued August 13, 2013; US10118958, entitled “Composition and method for the diagnosis and treatment of iron-related disorders”, issued November 6, 2018; US2010 / 0322941, entitled “Bone morphogenetic protein (BMP)-binding domains of proteins of the repulsive guidance molecule (RGM) protein family and functional fragments thereof, and use of same”, published December 23, 2010; US9040052, entitled “Precision Medicine By Targeting Rare Human PCSK9 Variants for Cholesterol Treatment”, issued May 26, 2015; and US2017 / 0029499, entitled “Methods for treating hepcidin-mediated disorders”, published February 2, 2017; and International Publication Nos. WO2007039256, entitled “Binding domains of proteins of the repulsive guidance molecule (rgm) protein family and functional fragments thereof, and their use,” published April 12, 2007; WO2015171691, entitled “Compositions and methods for growth factor modulation”, published November 12, 2015; WO2018 / 009624, entitled “Tgf-beta superfamily heteromultimers and uses thereof”, published January 11, 2018, and WO2020 / 086736, entitled “Rgmc-selective inhibitors and use thereof”, published April 30, 2020, the contents relating to anti-HJV or anti-RGMc antibodies of each of which are incorporated herein by reference. [000191] In some embodiments, the hemojuvelin antagonist is an antibody (e.g., hHA-001- hHA-012) specific for hemojuvelin and / or one or more proteins of the RGM protein family(e.g., RGMa, RGMb), as described herein in Table 1. In some embodiments, an anti-HJV antibody described herein also binds RGMa. Appropriate antibodies specific for hemojuvelin and / or one or more RGM proteins that may be useful in certain methods provided herein are provided for example, in U.S. Patent Nos. 10,118,958; and 8,507,435; U.S. Patent Publication Nos. US 2013 / 330343; US 2015 / 166672; and US 2017 / 029499; and International Publication Nos. WO 2015 / 171691; and WO 2018 / 009624, which are incorporated herein by reference. [000192] Provided herein, in some aspects, are antibodies that bind to human hemojuvelin (HJV) with high specificity and affinity. In some embodiments, the anti- HJV antibody described herein specifically binds to any extracellular epitope of a HJV or an epitope that becomes exposed to an antibody. In some embodiments, anti- HJV antibodies provided herein bind specifically to HJV from human, non-human primates, mouse, rat, etc. In some embodiments, anti- HJV antibodies provided herein bind to human HJV. In some embodiments, the anti- HJV antibody described herein binds to an amino acid segment of a human or non-human primate HJV. [000193] In some embodiments, the anti-HJV antibody described herein specifically binds to an epitope on human HJV. Human HJV is a 426 amino acid protein with a predicted N-terminal signal peptide of 31 amino acids and a C-terminal GPI-attachment signal of 45 amino acids. An exemplary human HJV amino acid sequence is set forth in SEQ ID NO: 128: MGEPGQSPSPRSSHGSPPTLSTLTLLLLLCGHAHSQCKILRCNAEYVSSTLSLRGGGSSGAL RGGGGGGRGGGVGSGGLCRALRSYALCTRRTARTCRGDLAFHSAVHGIEDLMIQHNCSRQGP TAPPPPRGPALPGAGSGLPAPDPCDYEGRFSRLHGRPPGFLHCASFGDPHVRSFHHHFHTCR VQGAWPLLDNDFLFVQATSSPMALGANATATRKLTIIFKNMQECIDQKVYQAEVDNLPVAFE DGSINGGDRPGGSSLSIQTANPGNHVEIQAAYIGTTIIIRQTAGQLSFSIKVAEDVAMAFSA EQDLQLCVGGCPPSQRLSRSERNRRGAITIDTARRLCKEGLPVEDAYFHSCVFDVLISGDPN FTVAAQAALEDARAFLPDLEKLHLFPSDAGVPLSSATLLAPLLSGLFVLWLCIQ (SEQ ID NO: 128) [000194] In some embodiments, the anti-HJV antibody described herein may bind to a fragment of a human HJV. The fragment of HJV may be between about 5 and about 425 amino acids, between about 10 and about 400 amino acids, between about 50 and about 350 amino acids, between about 100 and about 300 amino acids, between about 150 and about 250 amino acids, between about 200 and about 300 amino acids, or between about 75 and about 150 amino acids in length. The fragment may comprise a contiguous number of aminoacids from RGMc. An exemplary amino acid of a HJV fragment is set forth in SEQ ID NO: 123: QCKILRCNAEYVSSTLSLRGGGSSGALRGGGGGGRGGGVGSGGLCRALRSYALCTRRTARTC RGDLAFHSAVHGIEDLMIQHNCSRQGPTAPPPPRGPALPGAGSGLPAPDPCDYEGRFSRLHG RPPGFLHCASFGDPHVRSFHHHFHTCRVQGAWPLLDNDFLFVQATSSPMALGANATATRKLT IIFKNMQECIDQKVYQAEVDNLPVAFEDGSINGGDRPGGSSLSIQTANPGNHVEIQAAYIGT TIIIRQTAGQLSFSIKVAEDVAMAFSAEQDLQLCVGGCPPSQRLSRSERNRRGAITIDTARR LCKEGLPVEDAYFHSCVFDVLISGDPNFTVAAQAALEDARAFLPDLEKLHLFPSD (SEQ ID NO: 123) [000195] In some embodiments, the anti-HJV antibody described herein binds to different epitopes within a human HJV or a human HJV fragment. [000196] In some embodiments, the anti-HJV antibody interacts with an epitope within amino acids 160-190 of SEQ ID NO: 123. In some embodiments, the anti-HJV antibody interacts with an epitope having an amino acid sequence of amino acids 170-183 of SEQ ID NO: 123. In some embodiments, the anti-HJV antibody interacts with an epitope having the amino acid sequence of SSPMALGANATATR (SEQ ID NO: 121). In some embodiments, the anti-HJV antibody interacts with different segments within SSPMALGANATATR (SEQ ID NO: 121). In some embodiments, the anti-HJV antibody interacts with amino acids 170-171, amino acids 171-180, amino acids 180-182, and amino acids 182-183 of SEQ ID NO: 123. In some embodiments, the antibody interacts with amino acids 170 (S), 171(S), 180 (T), 182 (T) and 183 (R) of SEQ ID NO: 123. In some embodiments, hHA-008 interacts with the epitope SSPMALGANATATR (SEQ ID NO: 121). In some embodiments, hHA-008 interacts with amino acids 170 (S), 171(S), 180 (T), 182 (T) and 183 (R) of SEQ ID NO: 123. [000197] In some embodiments, the anti-HJV antibody interacts with an epitope within amino acids 160-190 of SEQ ID NO: 123 and / or amino acids 280-310 of SEQ ID NO: 123. In some embodiments, the anti-HJV antibody interacts with an epitope within amino acids 169-182 of SEQ ID NO: 123 and / or amino acids 289-300 of SEQ ID NO: 123. In some embodiments, the anti-HJV antibody interacts with an epitope within amino acids 169-182 of SEQ ID NO: 123 and amino acids 289-300 of SEQ ID NO: 123. In some embodiments, the anti-HJV antibody interacts with an epitope having the amino acid sequence of TSSPMALGANATAT (SEQ ID NO: 122) and amino acid sequence SQRLSRSERNRR (SEQ ID NO: 127). In some embodiments, the anti-HJV antibody interacts with different segments within TSSPMALGANATAT (SEQ ID NO: 122) and SQRLSRSERNRR (SEQ ID NO: 127). Insome embodiments, the anti-HJV antibody interacts with amino acids 169-171, amino acids 171-180, and amino acids 180-182 of SEQ ID NO: 123, and amino acids 289-293, amino acids 293-294, amino acids 294-295, amino acids 295-297 and amino acids 297-300 of SEQ ID NO: 123. In some embodiments, the antibody interacts with amino acids 169 (T), 170 (S), 171(S), 180 (T), 182 (T), 289 (S), 293 (S), 294 (R), 295(S), 297(R), and 300 (R) of SEQ ID NO: 123. In some embodiments, hHA-008-QL interacts with different segments within TSSPMALGANATAT (SEQ ID NO: 122) and SQRLSRSERNRR (SEQ ID NO: 127). In some embodiments, hHA-008-QL interacts with amino acids 169 (T), 170 (S), 171(S), 180 (T), 182 (T), 289 (S), 293 (S), 294 (R), 295(S), 297(R), and 300 (R) of SEQ ID NO: 123. [000198] In some embodiments, the anti-HJV antibodies described herein are affinity matured clones. In some embodiments, an anti- HJV antibody specifically binds a HJV (e.g., a human or non-human primate HJV) with binding affinity (e.g., as indicated by KD) of at least about 10-4M, 10-5M, 10-6M, 10-7M, 10-8M, 10-9M, 10-10M, 10-11M, 10-12M, 10-13M, or less. For example, the anti-HJV antibodies of the present disclosure can bind to a hemojuvelin protein (e.g., human hemojuvelin) with an affinity between 5 pM and 500 nM, e.g., between 50 pM and 100 nM, e.g., between 500 pM and 50 nM. The disclosure also includes antibodies that compete with any of the antibodies described herein for binding to a hemojuvelin protein (e.g., human hemojuvelin) and that have an affinity of 100 nM or lower (e.g., 80 nM or lower, 50 nM or lower, 20 nM or lower, 10 nM or lower, 500 pM or lower, 50 pM or lower, or 5 pM or lower). [000199] In some embodiments, in addition to binding HJV, an anti-HJV antibody described herein also binds RGMa. In some embodiments, in addition to being affinity matured for HJV, anti-HJV antibodies described herein are also affinity matured for RGMa. In some embodiments, an anti-HJV antibody specifically binds a RGMa (e.g., a human or non-human primate RGMa) with binding affinity (e.g., as indicated by KD) of at least about 10-4M, 10-5M, 10-6M, 10-7M, 10-8M, 10-9M, 10-10M, 10-11M, 10-12M, 10-13M, or less. For example, the anti-HJV antibodies of the present disclosure can bind to a RGMa protein (e.g., human RGMa) with an affinity between 5 pM and 500 nM, e.g., between 50 pM and 100 nM, e.g., between 500 pM and 50 nM. The disclosure also includes antibodies that compete with any of the antibodies described herein for binding to a RGMa protein (e.g., human RGMa) and that have an affinity of 100 nM or lower (e.g., 80 nM or lower, 50 nM or lower, 20 nM or lower, 10 nM or lower, 500 pM or lower, 50 pM or lower, or 5 pM or lower). [000200] The affinity and binding kinetics of the anti-HJV antibody can be tested using any suitable method including but not limited to biosensor technology (e.g., OCTET orBIACORE). In some embodiments, the anti- HJV antibodies described herein binds to HJV with a KD of sub-nanomolar range. In some embodiments, the anti- HJV antibodies described herein selectively binds to RGMc and / or RGMa, but not RGMb. [000201] Binding affinity (or binding specificity) can be determined by a variety of methods including equilibrium dialysis, equilibrium binding, gel filtration, ELISA, surface plasmon resonance (SPR), florescent activated cell sorting (FACS) or spectroscopy (e.g., using a fluorescence assay). Exemplary conditions for evaluating binding affinity are in HBS-P buffer (10 mM HEPES pH7.4, 150 mM NaCl, 0.005% (v / v) surfactant P20) and PBS buffer (10 mM PO4-3, 137 mM NaCl, and 2.7 mM KCl). These techniques can be used to measure the concentration of bound proteins as a function of target protein concentration. The concentration of bound protein ([Bound]) is generally related to the concentration of free target protein ([Free]) by the following equation: [Bound] = [Free] / (Kd+[Free]) [000202] It is not always necessary to make an exact determination of KA, though, since sometimes it is sufficient to obtain a quantitative measurement of affinity, e.g., determined using a method such as ELISA or FACS analysis, is proportional to KA, and thus can be used for comparisons, such as determining whether a higher affinity is, e.g., 2-fold higher, to obtain a qualitative measurement of affinity, or to obtain an inference of affinity, e.g., by activity in a functional assay, e.g., an in vitro or in vivo assay. [000203] The heavy chain (HC) and light chain (LC) sequences, heavy chain variable domain (VH) and light chain variable domain (VL), CDR sequences, and heavy chain and light chain constant region sequences of non-limiting examples of anti-HJV antibodies are provided in Table 1. Table 1. Examples of anti-HJV antibodies (CDRs according to the Kabat definition)[000204] In some embodiments, the N-terminus of the heavy chain of the anti-HJV antibody described herein is glutamic acid (E). In some embodiments, the glutamic acid can cyclize spontaneously to pyroglutamic acid by post-translational modification. Spontaneous cyclization of glutamic acid to pyroglutamic acid has been previously described, e.g., Chelius et al., Formation of Pyroglutamic Acid From N-terminal Glutamic Acid in Immunoglobulin Gamma Antibodies, Anal Chem. 2006;78(7):2370‐2376. In some embodiments, the N- terminus of the heavy chain of the anti-HJV antibody described herein is a pyroglutamic acid. In some embodiments, the anti-HJV antibodies having N-terminal pyroglutamic acid are impurities in the population of anti-HJV antibodies (e.g., less than 5%, less than 4%, less than 3%, less than 2%, less than 1%, less than 0.5%, less than 0.1%, less than 0.05%, or less than 0.01%) in the population of anti-HJV antibody. In some embodiments, the population of theanti-HJV antibodies comprises a mixture of anti-HJV antibodies having glutamic acid or pyroglutamic acid at the N-terminus of the heavy chain. [000205] In some embodiments, the anti-HJV antibodies of the present disclosure comprise one or more of the HC CDRs (e.g., HC CDR1, HC CDR2, or HC CDR3) amino acid sequences from any one of the anti-HJV antibodies selected from Table 1. In some embodiments, the anti-HJV antibodies of the present disclosure comprise the HC CDR1, HC CDR2, and HC CDR3 as provided for any one of the antibodies elected from Table 1. In some embodiments, the anti-HJV antibodies of the present disclosure comprises one or more of the LC CDRs (e.g., LC CDR1, LC CDR2, or LC CDR3) amino acid sequences from any one of the anti-HJV antibodies selected from Table 1. In some embodiments, the anti-HJV antibodies of the present disclosure comprise the LC CDR1, LC CDR2, and LC CDR3 as provided for any one of the anti-HJV antibodies selected from Table 1. [000206] In some embodiments, the anti-HJV antibodies of the present disclosure comprises the HC CDR1, HC CDR2, HC CDR3, LC CDR1, LC CDR2, and LC CDR3 as provided for any one of the anti-HJV antibodies selected from Table 1. In some embodiments, antibody heavy and light chain CDR3 domains may play a particularly important role in the binding specificity / affinity of an antibody for an antigen. Accordingly, the anti-HJV antibodies of the disclosure may include at least the heavy and / or light chain CDR3s of any one of the anti- HJV antibodies selected from Table 1. [000207] In some embodiments, the isolated anti-HJV antibody comprises a heavy chain variable region that comprises a heavy chain CDR1 (HC CDR1), a heavy chain CDR2 (HC CDR2), and a heavy chain CDR3 (HC CDR3). [000208] In some embodiments, following the Kabat definition, the HC CDR1 may comprise the amino acid sequence of X1YGMN (SEQ ID NO: 105), in which X1can be N or Y. Alternatively or in addition, the HC CDR2 may comprise the amino acid sequence of MIYYDSSX2KHYADSVKG (SEQ ID NO: 106), in which X2 can be E or D. Alternatively or in addition, the HC CDR3 may comprise the amino acid sequence of GX3TPDX4(SEQ ID NO: 107), in which X3 can be T or S, and X4 can be Y, V, or K. [000209] In some embodiments, following the Kabat definition, the anti-HJV antibody may comprise a light chain variable region that comprises a light chain CDR1 (LC CDR1), a light chain CDR2 (LC CDR2), and a light chain CDR3 (LC CDR3). In some embodiments, the LC CDR1 may comprise the amino acid sequence of RSSQSLX5X6SDGX7TFLX8 (SEQ ID NO: 108), in which X5 can be A or E, X6 can be T, S, E, or D, X7 can be D, Y, or G, and X8 can be E or H. Alternatively or in addition, the LC CDR2 may comprise the amino acidsequence of X9VSX10RFS (SEQ ID NO: 109), in which X9can be E, D or A, and X10can be N, S, T, E or H. Alternatively or in addition, the LC CDR3 may comprise the amino acid sequence of X11QX12TX13DPX14X15 (SEQ ID NO: 110), in which X11 can be F or M, X12 can be V or A, X13can be H or Y, X14can be M, L or V, and X15can be T or S. [000210] Also within the scope of the present disclosure are functional variants of any of the exemplary anti-HJV antibodies as disclosed herein. A functional variant may contain one or more amino acid residue variations in the VHand / or VL, or in one or more of the HC CDRs and / or one or more of the LC CDRs as relative to the reference antibody, while retaining substantially similar binding and biological activities (e.g., substantially similar binding affinity, binding specificity, inhibitory activity, anti-inflammatory activity, or a combination thereof) as the reference antibody. [000211] In some embodiments, any of the anti-HJV antibodies of the disclosure have one or more CDRs (e.g., HC CDR or LC CDR) sequences substantially similar to any of the HC CDR1, HC CDR2, HC CDR3, LC CDR1, LC CDR2, and / or LC CDR3 sequences from one of the anti-HJV antibodies selected from Table 1. In some embodiments, the position of one or more CDRs along the VH (e.g., HC CDR1, HC CDR2, or HC CDR3) and / or VL (e.g., LC CDR1, LC CDR2, or LC CDR3) region of an antibody described herein can vary by one, two, three, four, five, or six amino acid positions so long as immunospecific binding to hemojuvelin (e.g., human hemojuvelin) is maintained (e.g., substantially maintained, for example, at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, at least 95% of the binding of the original antibody from which it is derived). For example, in some embodiments, the position defining a CDR of any antibody described herein can vary by shifting the N-terminal and / or C-terminal boundary of the CDR by one, two, three, four, five, or six amino acids, relative to the CDR position of any one of the antibodies described herein, so long as immunospecific binding to hemojuvelin (e.g., human hemojuvelin) is maintained (e.g., substantially maintained, for example, at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, at least 95% of the binding of the original antibody from which it is derived). In another embodiment, the length of one or more CDRs along the VH (e.g., HC CDR1, HC CDR2, or HC CDR3) and / or VL (e.g., LC CDR1, LC CDR2, or LC CDR3) region of an antibody described herein can vary (e.g., be shorter or longer) by one, two, three, four, five, or more amino acids, so long as immunospecific binding to hemojuvelin (e.g., human hemojuvelin) is maintained (e.g., substantially maintained, for example, at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, at least 95% of the binding of the original antibody from which it is derived).[000212] Accordingly, in some embodiments, a HC CDR1, HC CDR2, HC CDR3, LC CDR1, LC CDR2, and / or LC CDR3 described herein may be one, two, three, four, five or more amino acids shorter than one or more of the CDRs described herein (e.g., CDRS from any of the anti-HJV antibodies selected from Table 1) so long as immunospecific binding to hemojuvelin (e.g., human hemojuvelin) is maintained (e.g., substantially maintained, for example, at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, at least 95% relative to the binding of the original antibody from which it is derived). In some embodiments, a HC CDR1, HC CDR2, HC CDR3, LC CDR1, LC CDR2, and / or LC CDR3 described herein may be one, two, three, four, five or more amino acids longer than one or more of the CDRs described herein (e.g., CDRS from any of the anti-HJV antibodies selected from Table 1) so long as immunospecific binding to hemojuvelin (e.g., human hemojuvelin) is maintained (e.g., substantially maintained, for example, at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, at least 95% relative to the binding of the original antibody from which it is derived). In some embodiments, the amino portion of a HC CDR1, HC CDR2, HC CDR3, LC CDR1, LC CDR2, and / or LC CDR3 described herein can be extended by one, two, three, four, five or more amino acids compared to one or more of the CDRs described herein (e.g., CDRS from any of the anti-HJV antibodies selected from Table 1) so long as immunospecific binding to hemojuvelin (e.g., human hemojuvelin) is maintained (e.g., substantially maintained, for example, at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, at least 95% relative to the binding of the original antibody from which it is derived). In some embodiments, the carboxy portion of a HC CDR1, HC CDR2, HC CDR3, LC CDR1, LC CDR2, and / or LC CDR3 described herein can be extended by one, two, three, four, five or more amino acids compared to one or more of the CDRs described herein (e.g., CDRS from any of the anti-HJV antibodies selected from Table 1) so long as immunospecific binding to hemojuvelin (e.g., human hemojuvelin) is maintained (e.g., substantially maintained, for example, at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, at least 95% relative to the binding of the original antibody from which it is derived). In some embodiments, the amino portion of a HC CDR1, HC CDR2, HC CDR3, LC CDR1, LC CDR2, and / or LC CDR3 described herein can be shortened by one, two, three, four, five or more amino acids compared to one or more of the CDRs described herein (e.g., CDRS from any of the anti-HJV antibodies selected from Table 1) so long as immunospecific binding to hemojuvelin (e.g., human hemojuvelin) is maintained (e.g., substantially maintained, for example, at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, at least 95% relative to the binding of the original antibody from which it is derived). In someembodiments, the carboxy portion of a HC CDR1, HC CDR2, HC CDR3, LC CDR1, LC CDR2, and / or LC CDR3 described herein can be shortened by one, two, three, four, five or more amino acids compared to one or more of the CDRs described herein (e.g., CDRS from any of the anti-HJV antibodies selected from Table 1) so long as immunospecific binding to hemojuvelin (e.g., human hemojuvelin) is maintained (e.g., substantially maintained, for example, at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, at least 95% relative to the binding of the original antibody from which it is derived). Any method can be used to ascertain whether immunospecific binding to hemojuvelin (e.g., human hemojuvelin) is maintained, for example, using binding assays and conditions described in the art. [000213] In some examples, any of the anti-HJV antibodies of the disclosure have one or more CDR (e.g., HC CDR or LC CDR) sequences substantially similar to any one of the anti- HJV antibodies selected from Table 1. For example, the antibodies may include one or more CDR sequence(s) from any of the anti-HJV antibodies selected from Table 1 containing up to 5, 4, 3, 2, or 1 amino acid residue variations as compared to the corresponding CDR region in any one of the CDRs provided herein (e.g., CDRs from any of the anti-HJV antibodies selected from Table 1) so long as immunospecific binding to hemojuvelin (e.g., human hemojuvelin) is maintained (e.g., substantially maintained, for example, at least 50%, at least 60%, at least 70%, at least 80%, at least 90%, at least 95% relative to the binding of the original antibody from which it is derived). In some embodiments, any of the amino acid variations in any of the CDRs provided herein may be conservative variations. Conservative variations can be introduced into the CDRs at positions where the residues are not likely to be involved in interacting with a hemojuvelin protein (e.g., a human hemojuvelin protein), for example, as determined based on a crystal structure. Some aspects of the disclosure provide anti-HJV antibodies that comprise one or more of the heavy chain variable (VH) and / or light chain variable (VL) domains provided herein. In some embodiments, any of the VH domains provided herein include one or more of the HC CDR sequences (e.g., HC CDR1, HC CDR2, and HC CDR3) provided herein, for example, any of the CDR-H sequences provided in any one of the anti-HJV selected from Table 1. In some embodiments, any of the VL domains provided herein include one or more of the CDR-L sequences (e.g., LC CDR1, LC CDR2, and LC CDR3) provided herein, for example, any of the LC CDR sequences provided in any one of the anti-HJV antibodies selected from Table 1. [000214] In some embodiments, the anti-HJV antibodies of the disclosure include any antibody that includes a heavy chain variable domain and / or a light chain variable domain of any one of the anti-HJV antibodies selected from Table 1, and variants thereof. In someembodiments, anti-HJV antibodies of the disclosure include any antibody that includes the heavy chain variable and light chain variable pairs of any anti-HJV antibodies selected from Table 1. [000215] Aspects of the disclosure provide anti-HJV antibodies having a heavy chain variable (VH) and / or a light chain variable (VL) domain amino acid sequence homologous to any of those described herein. In some embodiments, the anti-HJV antibody comprises a heavy chain variable sequence or a light chain variable sequence that is at least 75% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the heavy chain variable sequence and / or any light chain variable sequence of any one of the anti-HJV antibodies selected from Table 1. In some embodiments, the homologous heavy chain variable and / or a light chain variable amino acid sequences do not vary within any of the CDR sequences provided herein. For example, in some embodiments, the degree of sequence variation (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) may occur within a heavy chain variable and / or a light chain variable sequence excluding any of the CDR sequences provided herein. In some embodiments, any of the anti- HJV antibodies provided herein comprise a heavy chain variable sequence and a light chain variable sequence that comprises a framework sequence that is at least 75% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of any anti-HJV antibodies selected from Table 1. In some embodiments, any of the anti-HJV antibodies provided herein comprise a heavy chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VH of any one of anti-HJV antibodies selected from Table 1 and / or a light chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VL of any one of anti-HJV antibodies selected from Table 1. [000216] In some embodiments, an anti-HJV antibody of the present disclosure is a humanized antibody (e.g., a humanized variant containing one or more CDRs of Table 1). In some embodiments, an anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, a HC CDR3, a LC CDR1, a LC CDR2, and a LC CDR3 that are the same as theHC CDR1, HC CDR2, HC CDR3, LC CDR1, LC CDR2, and LC CDR3 shown in Table 1, and comprises a humanized heavy chain variable region and / or a humanized light chain variable region. In some embodiments, a humanized heavy chain variable and / or a humanized light chain variable amino acid sequences do not vary within any of the CDR sequences provided herein. For example, in some embodiments, the degree of sequence variation (e.g., at least 75%, at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) may occur within a heavy chain variable and / or a light chain variable sequence excluding any of the CDR sequences provided herein. In some embodiments, a humanized anti-HJV antibody provided herein comprises a heavy chain variable sequence and a light chain variable sequence that comprises a framework sequence that is at least 75%, at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99% identical to the framework sequence of any anti-HJV antibodies selected from Table 1. In some embodiments, a humanized heavy chain variable and / or a humanized light chain variable amino acid sequences do not vary within any of the CDR sequences provided herein. For example, in some embodiments, the number of amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) may occur within a heavy chain variable and / or a light chain variable sequence excluding any of the CDR sequences provided herein. In some embodiments, a humanized anti-HJV antibody provided herein comprises a heavy chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VH of any one of anti-HJV antibodies selected from Table 1 and / or a light chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VL of any one of anti-HJV antibodies selected from Table 1. [000217] Humanized antibodies are human immunoglobulins (recipient antibody) in which residues from a complementary determining region (CDR) of the recipient are replaced by residues from a CDR of a non-human species (donor antibody) such as mouse, rat, or rabbit having the desired specificity, affinity, and capacity. In some embodiments, Fv framework region (FR) residues of the human immunoglobulin are replaced by corresponding non- human residues. Furthermore, the humanized antibody may comprise residues that are found neither in the recipient antibody nor in the imported CDR or framework sequences but areincluded to further refine and optimize antibody performance. In general, the humanized antibody will comprise substantially all of at least one, and typically two, variable domains, in which all or substantially all of the CDR regions correspond to those of a non-human immunoglobulin and all or substantially all of the FR regions are those of a human immunoglobulin consensus sequence. The humanized antibody optimally also will comprise at least a portion of an immunoglobulin constant region or domain (Fc), typically that of a human immunoglobulin. Antibodies may have Fc regions modified as described in WO 99 / 58572. Other forms of humanized antibodies have one or more CDRs (one, two, three, four, five, six) which are altered with respect to the original antibody, which are also termed one or more CDRs derived from one or more CDRs from the original antibody. Humanized antibodies may also involve affinity maturation. [000218] In some embodiments, humanization is achieved by grafting the CDRs (e.g., as shown in Table 1) into the human variable domains (e.g., IGKV1-NL1*01 and IGHV1-3*01 human variable domain). In some embodiments, the anti-HJV antibody of the present disclosure is a humanized variant comprising one or more amino acid substitutions (e.g., in the VH framework region) as compared with any one of the VHs listed in Table 1, and / or one or more amino acid substitutions (e.g., in the VL framework region) as compared with any one of the VLs listed in Table 1. [000219] In some embodiments, the anti-HJV antibody of the present disclosure is a humanized antibody comprising a VH containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VH of any of the anti-HJV antibodies listed in Table 1. Alternatively or in addition, the anti-HJV antibody of the present disclosure is a humanized antibody comprising a VL containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VL of any one of the anti-HJV antibodies listed in Table 1. [000220] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, HC CDR2 and HC CDR3 of a heavy chain variable domain having the amino acid sequence of SEQ ID NO: 7. Alternatively, or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, LC CDR2 and LC CDR3 of a light chain variable domain having the amino acid sequence of SEQ ID NO: 8. [000221] In some embodiments, according to the Kabat definition system, the anti-HJV antibody of the present disclosure comprises a HC CDR1 having the amino acid sequence of SEQ ID NO: 1, a HC CDR2 having the amino acid sequence of SEQ ID NO: 2, a HC CDR3having the amino acid sequence of SEQ ID NO: 3, a LC CDR1 having the amino acid sequence of SEQ ID NO: 4, a LC CDR2 having the amino acid sequence of SEQ ID NO: 5, and a LC CDR3 having the amino acid sequence of SEQ ID NO: 6. [000222] In some embodiments, anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 1, HC CDR2 having the amino acid sequence of SEQ ID NO: 2, and HC CDR3 having the amino acid sequence of SEQ ID NO: 3. “Collectively,” as used anywhere in the present disclosure, means that the total number of amino acid variations in all of the three heavy chain CDRs is within the defined range. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LC CDR2, and a LC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2 or 1 amino acid variation) as compared with the LC CDR1 having the amino acid sequence of SEQ ID NO: 4, LC CDR2 having the amino acid sequence of SEQ ID NO: 5, and LC CDR3 having the amino acid sequence of SEQ ID NO: 6. [000223] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the HC CDR1 having the amino acid sequence of SEQ ID NO: 1, HC CDR2 having the amino acid sequence of SEQ ID NO: 2, and HC CDR3 having the amino acid sequence of SEQ ID NO: 3. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LC CDR2, and a LC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the to the LC CDR1 having the amino acid sequence of SEQ ID NO: 4, LC CDR2 having the amino acid sequence of SEQ ID NO: 5, and LC CDR3 having the amino acid sequence of SEQ ID NO: 6. [000224] In some embodiments, the anti-HJV antibody of the present disclosure comprises: a HC CDR1 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 1; a HC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR2 having the amino acid sequence of SEQ ID NO: 2; and / or a HC CDR3 having no more than 3 amino acid variations (e.g., nomore than 3, 2, or 1 amino acid variation) as compared with the HC CDR3 having the amino acid sequence of SEQ ID NO: 3. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises: a LC CDR1 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR1 having the amino acid sequence of SEQ ID NO: 4; a LC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR2 having the amino acid sequence of SEQ ID NO: 5; and / or a LC CDR3 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR3 having the amino acid sequence of SEQ ID NO: 6. [000225] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising the amino acid sequence of SEQ ID NO: 7. Alternatively, or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising the amino acid sequence of SEQ ID NO: 8. [000226] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VH as set forth in SEQ ID NO: 7. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VL as set forth in SEQ ID NO: 8. In some embodiments, the number of amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) may occur within a VH of SEQ ID NO: 7 and / or a VL of SEQ ID NO: 8 excluding any of the CDR sequences therein. In some embodiments, an anti-HJV antibodies provided herein comprise a heavy chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VH of SEQ ID NO: 7, and / or a light chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VL of SEQ ID NO: 8. [000227] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the VH as set forth in SEQ ID NO: 7.Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the VL as set forth in SEQ ID NO: 8.In some embodiments, the degree of sequence variation (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) may occur within a VH of SEQ ID NO: 7, and / or a VL of SEQ ID NO: 8 excluding any of the CDR sequences therein. In some embodiments, an anti-HJV antibody provided herein comprise a heavy chain variable sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VH of SEQ ID NO: 7, and / or a light chain variable sequence that comprises a framework sequence that at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VL of SEQ ID NO: 8. [000228] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, HC CDR2 and HC CDR3 of a heavy chain variable domain having the amino acid sequence of SEQ ID NO: 7. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, LC CDR2 and LC CDR3 of a light chain variable domain having the amino acid sequence of SEQ ID NO: 30. [000229] In some embodiments, according to the Kabat definition system, the anti-HJV antibody of the present disclosure comprises a HC CDR1 having the amino acid sequence of SEQ ID NO: 1, a HC CDR2 having the amino acid sequence of SEQ ID NO: 2, a HC CDR3 having the amino acid sequence of SEQ ID NO: 3, a LC CDR1 having the amino acid sequence of SEQ ID NO: 4, a LC CDR2 having the amino acid sequence of SEQ ID NO: 49, and a LC CDR3 having the amino acid sequence of SEQ ID NO: 24. [000230] In some embodiments, anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 1, HC CDR2 having the amino acid sequence of SEQ ID NO: 2, and HC CDR3 having the amino acid sequence of SEQ ID NO: 3. “Collectively,” as used anywhere in the present disclosure, means that the total number ofamino acid variations in all of the three heavy chain CDRs is within the defined range. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LC CDR2, and a LC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2 or 1 amino acid variation) as compared with the LC CDR1 having the amino acid sequence of SEQ ID NO: 4, LC CDR2 having the amino acid sequence of SEQ ID NO: 49, and LC CDR3 having the amino acid sequence of SEQ ID NO: 24. [000231] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the HC CDR1 having the amino acid sequence of SEQ ID NO: 1, HC CDR2 having the amino acid sequence of SEQ ID NO: 2, and HC CDR3 having the amino acid sequence of SEQ ID NO: 3. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LC CDR2, and a LC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the to the LC CDR1 having the amino acid sequence of SEQ ID NO: 4, LC CDR2 having the amino acid sequence of SEQ ID NO: 49, and LC CDR3 having the amino acid sequence of SEQ ID NO: 24. [000232] In some embodiments, the anti-HJV antibody of the present disclosure comprises: a HC CDR1 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 1; a HC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR2 having the amino acid sequence of SEQ ID NO: 2; and / or a HC CDR3 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR3 having the amino acid sequence of SEQ ID NO: 3. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises: a LC CDR1 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR1 having the amino acid sequence of SEQ ID NO: 4; a LC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR2 having the amino acid sequence of SEQ ID NO: 49; and / or a LC CDR3 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR3 having the amino acid sequence of SEQ ID NO: 24.[000233] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising the amino acid sequence of SEQ ID NO: 7. Alternatively, or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising the amino acid sequence of SEQ ID NO: 30. [000234] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VH as set forth in SEQ ID NO: 7. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VL as set forth in SEQ ID NO: 30. In some embodiments, the number of amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) may occur within a VH of SEQ ID NO: 7 and / or a VL of SEQ ID NO: 30 excluding any of the CDR sequences therein. In some embodiments, an anti-HJV antibodies provided herein comprise a heavy chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VH of SEQ ID NO: 7, and / or a light chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VL of SEQ ID NO: 30. [000235] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the VH as set forth in SEQ ID NO: 7. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the VL as set forth in SEQ ID NO: 30. In some embodiments, the degree of sequence variation (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) may occur within a VH of SEQ ID NO: 7, and / or a VL of SEQ ID NO: 30 excluding any of the CDR sequences therein. In some embodiments, an anti-HJV antibody provided herein comprise a heavy chain variable sequence that is atleast 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VH of SEQ ID NO: 7, and / or a light chain variable sequence that comprises a framework sequence that at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VL of SEQ ID NO: 30. [000236] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, HC CDR2 and HC CDR3 of a heavy chain variable domain having the amino acid sequence of SEQ ID NO: 7. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, LC CDR2 and LC CDR3 of a light chain variable domain having the amino acid sequence of SEQ ID NO: 31. [000237] In some embodiments, according to the Kabat definition system, the anti-HJV antibody of the present disclosure comprises a HC CDR1 having the amino acid sequence of SEQ ID NO: 1, a HC CDR2 having the amino acid sequence of SEQ ID NO: 2, a HC CDR3 having the amino acid sequence of SEQ ID NO: 3, a LC CDR1 having the amino acid sequence of SEQ ID NO: 4, a LC CDR2 having the amino acid sequence of SEQ ID NO: 18, and a LC CDR3 having the amino acid sequence of SEQ ID NO: 25. [000238] In some embodiments, anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 1, HC CDR2 having the amino acid sequence of SEQ ID NO: 2, and HC CDR3 having the amino acid sequence of SEQ ID NO: 3. “Collectively,” as used anywhere in the present disclosure, means that the total number of amino acid variations in all of the three heavy chain CDRs is within the defined range. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LC CDR2, and a LC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2 or 1 amino acid variation) as compared with the LC CDR1 having the amino acid sequence of SEQ ID NO: 4, LC CDR2 having the amino acid sequence of SEQ ID NO: 18, and LC CDR3 having the amino acid sequence of SEQ ID NO: 25. [000239] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%,at least 96%, at least 97%, at least 98%, or at least 99%) identical to the HC CDR1 having the amino acid sequence of SEQ ID NO: 1, HC CDR2 having the amino acid sequence of SEQ ID NO: 2, and HC CDR3 having the amino acid sequence of SEQ ID NO: 3. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LC CDR2, and a LC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the to the LC CDR1 having the amino acid sequence of SEQ ID NO: 4, LC CDR2 having the amino acid sequence of SEQ ID NO: 18, and LC CDR3 having the amino acid sequence of SEQ ID NO: 25. [000240] In some embodiments, the anti-HJV antibody of the present disclosure comprises: a HC CDR1 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 1; a HC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR2 having the amino acid sequence of SEQ ID NO: 2; and / or a HC CDR3 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR3 having the amino acid sequence of SEQ ID NO: 3. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises: a LC CDR1 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR1 having the amino acid sequence of SEQ ID NO: 4; a LC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR2 having the amino acid sequence of SEQ ID NO: 18; and / or a LC CDR3 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR3 having the amino acid sequence of SEQ ID NO: 25 [000241] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising the amino acid sequence of SEQ ID NO: 7. Alternatively, or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising the amino acid sequence of SEQ ID NO: 31 [000242] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VH as set forth in SEQ ID NO: 7. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acidvariation) as compared with the VL as set forth in SEQ ID NO: 31. In some embodiments, the number of amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) may occur within a VH of SEQ ID NO: 7 and / or a VL of SEQ ID NO: 31 excluding any of the CDR sequences therein. In some embodiments, an anti-HJV antibodies provided herein comprise a heavy chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VH of SEQ ID NO: 7, and / or a light chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VL of SEQ ID NO: 31. [000243] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the VH as set forth in SEQ ID NO: 7. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the VL as set forth in SEQ ID NO: 31. In some embodiments, the degree of sequence variation (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) may occur within a VH of SEQ ID NO: 7, and / or a VL of SEQ ID NO: 31 excluding any of the CDR sequences therein. In some embodiments, an anti-HJV antibody provided herein comprise a heavy chain variable sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VH of SEQ ID NO: 7, and / or a light chain variable sequence that comprises a framework sequence that at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VL of SEQ ID NO: 31. [000244] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, HC CDR2 and HC CDR3 of a heavy chain variable domain having the amino acid sequence of SEQ ID NO: 7. Alternatively or in addition, the anti-HJV antibody of thepresent disclosure comprises a LC CDR1, LC CDR2 and LC CDR3 of a light chain variable domain having the amino acid sequence of SEQ ID NO: 32. [000245] In some embodiments, according to the Kabat definition system, the anti-HJV antibody of the present disclosure comprises a HC CDR1 having the amino acid sequence of SEQ ID NO: 1, a HC CDR2 having the amino acid sequence of SEQ ID NO: 2, a HC CDR3 having the amino acid sequence of SEQ ID NO: 3, a LC CDR1 having the amino acid sequence of SEQ ID NO: 14, a LC CDR2 having the amino acid sequence of SEQ ID NO: 19, and a LC CDR3 having the amino acid sequence of SEQ ID NO: 25. [000246] In some embodiments, anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 1, HC CDR2 having the amino acid sequence of SEQ ID NO: 2, and HC CDR3 having the amino acid sequence of SEQ ID NO: 3. “Collectively,” as used anywhere in the present disclosure, means that the total number of amino acid variations in all of the three heavy chain CDRs is within the defined range. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LC CDR2, and a LC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2 or 1 amino acid variation) as compared with the LC CDR1 having the amino acid sequence of SEQ ID NO: 14, LC CDR2 having the amino acid sequence of SEQ ID NO: 19, and LC CDR3 having the amino acid sequence of SEQ ID NO: 25. [000247] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the HC CDR1 having the amino acid sequence of SEQ ID NO: 1, HC CDR2 having the amino acid sequence of SEQ ID NO: 2, and HC CDR3 having the amino acid sequence of SEQ ID NO: 3. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LC CDR2, and a LC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the to the LC CDR1 having the amino acid sequence of SEQ ID NO: 14, LC CDR2 having the amino acid sequence of SEQ ID NO: 19, and LC CDR3 having the amino acid sequence of SEQ ID NO: 25.[000248] In some embodiments, the anti-HJV antibody of the present disclosure comprises: a HC CDR1 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 1; a HC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR2 having the amino acid sequence of SEQ ID NO: 2; and / or a HC CDR3 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR3 having the amino acid sequence of SEQ ID NO: 3. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises: a LC CDR1 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR1 having the amino acid sequence of SEQ ID NO: 14; a LC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR2 having the amino acid sequence of SEQ ID NO: 19; and / or a LC CDR3 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR3 having the amino acid sequence of SEQ ID NO: 25. [000249] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising the amino acid sequence of SEQ ID NO: 7. Alternatively, or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising the amino acid sequence of SEQ ID NO: 32. [000250] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VH as set forth in SEQ ID NO: 7. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VL as set forth in SEQ ID NO: 32. In some embodiments, the number of amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) may occur within a VH of SEQ ID NO: 7 and / or a VL of SEQ ID NO: 32 excluding any of the CDR sequences therein. In some embodiments, an anti-HJV antibodies provided herein comprise a heavy chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VH of SEQ ID NO: 7, and / or a light chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10,9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VL of SEQ ID NO: 32. [000251] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the VH as set forth in SEQ ID NO: 7. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the VL as set forth in SEQ ID NO: 32. In some embodiments, the degree of sequence variation (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) may occur within a VH of SEQ ID NO: 7, and / or a VL of SEQ ID NO: 32 excluding any of the CDR sequences therein. In some embodiments, an anti-HJV antibody provided herein comprise a heavy chain variable sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VH of SEQ ID NO: 7, and / or a light chain variable sequence that comprises a framework sequence that at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VL of SEQ ID NO: 32. [000252] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, HC CDR2 and HC CDR3 of a heavy chain variable domain having the amino acid sequence of SEQ ID NO: 7. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, LC CDR2 and LC CDR3 of a light chain variable domain having the amino acid sequence of SEQ ID NO: 33. [000253] In some embodiments, according to the Kabat definition system, the anti-HJV antibody of the present disclosure comprises a HC CDR1 having the amino acid sequence of SEQ ID NO: 1, a HC CDR2 having the amino acid sequence of SEQ ID NO: 2, a HC CDR3 having the amino acid sequence of SEQ ID NO: 3, a LC CDR1 having the amino acid sequence of SEQ ID NO: 15, a LC CDR2 having the amino acid sequence of SEQ ID NO: 20, and a LC CDR3 having the amino acid sequence of SEQ ID NO: 26.[000254] In some embodiments, anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 1, HC CDR2 having the amino acid sequence of SEQ ID NO: 2, and HC CDR3 having the amino acid sequence of SEQ ID NO: 3. “Collectively,” as used anywhere in the present disclosure, means that the total number of amino acid variations in all of the three heavy chain CDRs is within the defined range. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LC CDR2, and a LC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2 or 1 amino acid variation) as compared with the LC CDR1 having the amino acid sequence of SEQ ID NO: 15, LC CDR2 having the amino acid sequence of SEQ ID NO: 20, and LC CDR3 having the amino acid sequence of SEQ ID NO: 26. [000255] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the HC CDR1 having the amino acid sequence of SEQ ID NO: 1, HC CDR2 having the amino acid sequence of SEQ ID NO: 2, and HC CDR3 having the amino acid sequence of SEQ ID NO: 3. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LC CDR2, and a LC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the to the LC CDR1 having the amino acid sequence of SEQ ID NO: 15, LC CDR2 having the amino acid sequence of SEQ ID NO: 20, and LC CDR3 having the amino acid sequence of SEQ ID NO: 26. [000256] In some embodiments, the anti-HJV antibody of the present disclosure comprises: a HC CDR1 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 1; a HC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR2 having the amino acid sequence of SEQ ID NO: 2; and / or a HC CDR3 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR3 having the amino acid sequence of SEQ ID NO: 3. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises: a LC CDR1 having no more than 3 amino acid variations (e.g.,no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR1 having the amino acid sequence of SEQ ID NO: 15; a LC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR2 having the amino acid sequence of SEQ ID NO: 20; and / or a LC CDR3 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR3 having the amino acid sequence of SEQ ID NO: 26. [000257] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising the amino acid sequence of SEQ ID NO: 7. Alternatively, or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising the amino acid sequence of SEQ ID NO: 33. [000258] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VH as set forth in SEQ ID NO: 7. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VL as set forth in SEQ ID NO: 33. In some embodiments, the number of amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) may occur within a VH of SEQ ID NO: 7 and / or a VL of SEQ ID NO: 33 excluding any of the CDR sequences therein. In some embodiments, an anti-HJV antibodies provided herein comprise a heavy chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VH of SEQ ID NO: 7, and / or a light chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VL of SEQ ID NO: 33. [000259] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the VH as set forth in SEQ ID NO: 7. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, atleast 97%, at least 98%, or at least 99%) identical to the VL as set forth in SEQ ID NO: 33. In some embodiments, the degree of sequence variation (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) may occur within a VH of SEQ ID NO: 7, and / or a VL of SEQ ID NO: 33 excluding any of the CDR sequences therein. In some embodiments, an anti-HJV antibody provided herein comprise a heavy chain variable sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VH of SEQ ID NO: 7, and / or a light chain variable sequence that comprises a framework sequence that at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VL of SEQ ID NO: 33. [000260] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, HC CDR2 and HC CDR3 of a heavy chain variable domain having the amino acid sequence of SEQ ID NO: 34. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, LC CDR2 and LC CDR3 of a light chain variable domain having the amino acid sequence of SEQ ID NO: 35. [000261] In some embodiments, according to the Kabat definition system, the anti-HJV antibody of the present disclosure comprises a HC CDR1 having the amino acid sequence of SEQ ID NO: 9, a HC CDR2 having the amino acid sequence of SEQ ID NO: 2, a HC CDR3 having the amino acid sequence of SEQ ID NO: 3, a LC CDR1 having the amino acid sequence of SEQ ID NO: 16, a LC CDR2 having the amino acid sequence of SEQ ID NO: 21, and a LC CDR3 having the amino acid sequence of SEQ ID NO: 27. [000262] In some embodiments, anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 9, HC CDR2 having the amino acid sequence of SEQ ID NO: 2, and HC CDR3 having the amino acid sequence of SEQ ID NO: 3. “Collectively,” as used anywhere in the present disclosure, means that the total number of amino acid variations in all of the three heavy chain CDRs is within the defined range. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LC CDR2, and a LC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2 or 1 amino acid variation) as compared with the LCCDR1 having the amino acid sequence of SEQ ID NO: 16, LC CDR2 having the amino acid sequence of SEQ ID NO: 21, and LC CDR3 having the amino acid sequence of SEQ ID NO: 27. [000263] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the HC CDR1 having the amino acid sequence of SEQ ID NO: 9, HC CDR2 having the amino acid sequence of SEQ ID NO: 2, and HC CDR3 having the amino acid sequence of SEQ ID NO: 3. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LC CDR2, and a LC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the to the LC CDR1 having the amino acid sequence of SEQ ID NO: 16, LC CDR2 having the amino acid sequence of SEQ ID NO: 21, and LC CDR3 having the amino acid sequence of SEQ ID NO: 27. [000264] In some embodiments, the anti-HJV antibody of the present disclosure comprises: a HC CDR1 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 9; a HC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR2 having the amino acid sequence of SEQ ID NO: 2; and / or a HC CDR3 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR3 having the amino acid sequence of SEQ ID NO: 3. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises: a LC CDR1 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR1 having the amino acid sequence of SEQ ID NO: 16; a LC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR2 having the amino acid sequence of SEQ ID NO: 21; and / or a LC CDR3 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR3 having the amino acid sequence of SEQ ID NO: 27. [000265] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising the amino acid sequence of SEQ ID NO: 34. Alternatively, or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising the amino acid sequence of SEQ ID NO: 35.[000266] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VH as set forth in SEQ ID NO: 34. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VL as set forth in SEQ ID NO: 35. In some embodiments, the number of amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) may occur within a VH of SEQ ID NO: 34 and / or a VL of SEQ ID NO: 35 excluding any of the CDR sequences therein. In some embodiments, an anti-HJV antibodies provided herein comprise a heavy chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VH of SEQ ID NO: 34, and / or a light chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VL of SEQ ID NO: 35. [000267] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the VH as set forth in SEQ ID NO: 34. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the VL as set forth in SEQ ID NO: 35. In some embodiments, the degree of sequence variation (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) may occur within a VH of SEQ ID NO: 34, and / or a VL of SEQ ID NO: 35 excluding any of the CDR sequences therein. In some embodiments, an anti-HJV antibody provided herein comprise a heavy chain variable sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VH of SEQ ID NO: 34, and / or a light chain variable sequence that comprises a framework sequence that at least 80% (e.g., at least 80%,at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VL of SEQ ID NO: 35. [000268] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, HC CDR2 and HC CDR3 of a heavy chain variable domain having the amino acid sequence of SEQ ID NO: 36. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, LC CDR2 and LC CDR3 of a light chain variable domain having the amino acid sequence of SEQ ID NO: 37. [000269] In some embodiments, according to the Kabat definition system, the anti-HJV antibody of the present disclosure comprises a HC CDR1 having the amino acid sequence of SEQ ID NO: 1, a HC CDR2 having the amino acid sequence of SEQ ID NO: 10, a HC CDR3 having the amino acid sequence of SEQ ID NO: 11, a LC CDR1 having the amino acid sequence of SEQ ID NO: 17, a LC CDR2 having the amino acid sequence of SEQ ID NO: 18, and a LC CDR3 having the amino acid sequence of SEQ ID NO: 28. [000270] In some embodiments, anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 1, HC CDR2 having the amino acid sequence of SEQ ID NO: 10, and HC CDR3 having the amino acid sequence of SEQ ID NO: 11. “Collectively,” as used anywhere in the present disclosure, means that the total number of amino acid variations in all of the three heavy chain CDRs is within the defined range. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LC CDR2, and a LC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2 or 1 amino acid variation) as compared with the LC CDR1 having the amino acid sequence of SEQ ID NO: 17, LC CDR2 having the amino acid sequence of SEQ ID NO: 18, and LC CDR3 having the amino acid sequence of SEQ ID NO: 28. [000271] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the HC CDR1 having the amino acid sequence of SEQ ID NO: 1, HC CDR2 having the amino acid sequence of SEQ ID NO: 10, and HC CDR3 having the amino acid sequence of SEQ ID NO: 11. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LCCDR2, and a LC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the to the LC CDR1 having the amino acid sequence of SEQ ID NO: 17, LC CDR2 having the amino acid sequence of SEQ ID NO: 18, and LC CDR3 having the amino acid sequence of SEQ ID NO: 28. [000272] In some embodiments, the anti-HJV antibody of the present disclosure comprises: a HC CDR1 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 1; a HC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR2 having the amino acid sequence of SEQ ID NO: 10; and / or a HC CDR3 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR3 having the amino acid sequence of SEQ ID NO: 11. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises: a LC CDR1 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR1 having the amino acid sequence of SEQ ID NO: 17; a LC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR2 having the amino acid sequence of SEQ ID NO: 18; and / or a LC CDR3 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR3 having the amino acid sequence of SEQ ID NO: 28. [000273] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising the amino acid sequence of SEQ ID NO: 36. Alternatively, or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising the amino acid sequence of SEQ ID NO: 37. [000274] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VH as set forth in SEQ ID NO: 36. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VL as set forth in SEQ ID NO: 37. In some embodiments, the number of amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) may occur within a VH of SEQ ID NO: 36 and / or a VL of SEQ ID NO: 37 excluding any of the CDR sequences therein. In someembodiments, an anti-HJV antibodies provided herein comprise a heavy chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VH of SEQ ID NO: 36, and / or a light chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VL of SEQ ID NO: 37. [000275] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the VH as set forth in SEQ ID NO: 36. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the VL as set forth in SEQ ID NO: 37. In some embodiments, the degree of sequence variation (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) may occur within a VH of SEQ ID NO: 36, and / or a VL of SEQ ID NO: 37 excluding any of the CDR sequences therein. In some embodiments, an anti-HJV antibody provided herein comprise a heavy chain variable sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VH of SEQ ID NO: 36, and / or a light chain variable sequence that comprises a framework sequence that at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VL of SEQ ID NO: 37. [000276] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, HC CDR2 and HC CDR3 of a heavy chain variable domain having the amino acid sequence of SEQ ID NO: 38. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, LC CDR2 and LC CDR3 of a light chain variable domain having the amino acid sequence of SEQ ID NO: 39. [000277] In some embodiments, according to the Kabat definition system, the anti-HJV antibody of the present disclosure comprises a HC CDR1 having the amino acid sequence ofSEQ ID NO: 1, a HC CDR2 having the amino acid sequence of SEQ ID NO: 2, a HC CDR3 having the amino acid sequence of SEQ ID NO: 3, a LC CDR1 having the amino acid sequence of SEQ ID NO: 17, a LC CDR2 having the amino acid sequence of SEQ ID NO: 5, and a LC CDR3 having the amino acid sequence of SEQ ID NO: 27. [000278] In some embodiments, anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 1, HC CDR2 having the amino acid sequence of SEQ ID NO: 2, and HC CDR3 having the amino acid sequence of SEQ ID NO: 3. “Collectively,” as used anywhere in the present disclosure, means that the total number of amino acid variations in all of the three heavy chain CDRs is within the defined range. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LC CDR2, and a LC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2 or 1 amino acid variation) as compared with the LC CDR1 having the amino acid sequence of SEQ ID NO: 17, LC CDR2 having the amino acid sequence of SEQ ID NO: 5, and LC CDR3 having the amino acid sequence of SEQ ID NO: 27. [000279] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the HC CDR1 having the amino acid sequence of SEQ ID NO: 1, HC CDR2 having the amino acid sequence of SEQ ID NO: 2, and HC CDR3 having the amino acid sequence of SEQ ID NO: 3. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LC CDR2, and a LC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the to the LC CDR1 having the amino acid sequence of SEQ ID NO: 17, LC CDR2 having the amino acid sequence of SEQ ID NO: 5, and LC CDR3 having the amino acid sequence of SEQ ID NO: 27. [000280] In some embodiments, the anti-HJV antibody of the present disclosure comprises: a HC CDR1 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 1; a HC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR2 having the amino acid sequence ofSEQ ID NO: 2; and / or a HC CDR3 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR3 having the amino acid sequence of SEQ ID NO: 3. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises: a LC CDR1 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR1 having the amino acid sequence of SEQ ID NO: 17; a LC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR2 having the amino acid sequence of SEQ ID NO: 5; and / or a LC CDR3 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR3 having the amino acid sequence of SEQ ID NO: 27. [000281] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising the amino acid sequence of SEQ ID NO: 38. Alternatively, or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising the amino acid sequence of SEQ ID NO: 39. [000282] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VH as set forth in SEQ ID NO: 38. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VL as set forth in SEQ ID NO: 39. In some embodiments, the number of amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) may occur within a VH of SEQ ID NO: 38 and / or a VL of SEQ ID NO: 39 excluding any of the CDR sequences therein. In some embodiments, an anti-HJV antibodies provided herein comprise a heavy chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VH of SEQ ID NO: 38, and / or a light chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VL of SEQ ID NO: 39. [000283] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%,at least 97%, at least 98%, or at least 99%) identical to the VH as set forth in SEQ ID NO: 38. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the VL as set forth in SEQ ID NO: 39. In some embodiments, the degree of sequence variation (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) may occur within a VH of SEQ ID NO: 38, and / or a VL of SEQ ID NO: 39 excluding any of the CDR sequences therein. In some embodiments, an anti-HJV antibody provided herein comprise a heavy chain variable sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VH of SEQ ID NO: 38, and / or a light chain variable sequence that comprises a framework sequence that at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VL of SEQ ID NO: 39. [000284] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, HC CDR2 and HC CDR3 of a heavy chain variable domain having the amino acid sequence of SEQ ID NO: 38. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, LC CDR2 and LC CDR3 of a light chain variable domain having the amino acid sequence of SEQ ID NO: 41. [000285] In some embodiments, according to the Kabat definition system, the anti-HJV antibody of the present disclosure comprises a HC CDR1 having the amino acid sequence of SEQ ID NO: 1, a HC CDR2 having the amino acid sequence of SEQ ID NO: 2, a HC CDR3 having the amino acid sequence of SEQ ID NO: 3, a LC CDR1 having the amino acid sequence of SEQ ID NO: 50, a LC CDR2 having the amino acid sequence of SEQ ID NO: 22, and a LC CDR3 having the amino acid sequence of SEQ ID NO: 28. [000286] In some embodiments, anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 1, HC CDR2 having the amino acid sequence of SEQ ID NO: 2, and HC CDR3 having the amino acid sequence of SEQ ID NO: 3. “Collectively,” as used anywhere in the present disclosure, means that the total number ofamino acid variations in all of the three heavy chain CDRs is within the defined range. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LC CDR2, and a LC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2 or 1 amino acid variation) as compared with the LC CDR1 having the amino acid sequence of SEQ ID NO: 50, LC CDR2 having the amino acid sequence of SEQ ID NO: 22, and LC CDR3 having the amino acid sequence of SEQ ID NO: 28. [000287] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the HC CDR1 having the amino acid sequence of SEQ ID NO: 1, HC CDR2 having the amino acid sequence of SEQ ID NO: 2, and HC CDR3 having the amino acid sequence of SEQ ID NO: 3. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LC CDR2, and a LC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the to the LC CDR1 having the amino acid sequence of SEQ ID NO: 50, LC CDR2 having the amino acid sequence of SEQ ID NO: 22, and LC CDR3 having the amino acid sequence of SEQ ID NO: 28. [000288] In some embodiments, the anti-HJV antibody of the present disclosure comprises: a HC CDR1 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 1; a HC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR2 having the amino acid sequence of SEQ ID NO: 2; and / or a HC CDR3 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR3 having the amino acid sequence of SEQ ID NO: 3. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises: a LC CDR1 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR1 having the amino acid sequence of SEQ ID NO: 50; a LC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR2 having the amino acid sequence of SEQ ID NO: 22; and / or a LC CDR3 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR3 having the amino acid sequence of SEQ ID NO: 28.[000289] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising the amino acid sequence of SEQ ID NO: 38. Alternatively, or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising the amino acid sequence of SEQ ID NO: 41. [000290] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VH as set forth in SEQ ID NO: 38. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VL as set forth in SEQ ID NO: 41. In some embodiments, the number of amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) may occur within a VH of SEQ ID NO: 38 and / or a VL of SEQ ID NO: 41 excluding any of the CDR sequences therein. In some embodiments, an anti-HJV antibodies provided herein comprise a heavy chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VH of SEQ ID NO: 38, and / or a light chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VL of SEQ ID NO: 41. [000291] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the VH as set forth in SEQ ID NO: 38. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the VL as set forth in SEQ ID NO: 41. In some embodiments, the degree of sequence variation (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) may occur within a VH of SEQ ID NO: 38, and / or a VL of SEQ ID NO: 41 excluding any of the CDR sequences therein. In some embodiments, an anti-HJV antibody provided herein comprise a heavy chain variablesequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VH of SEQ ID NO: 38, and / or a light chain variable sequence that comprises a framework sequence that at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VL of SEQ ID NO: 41. [000292] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, HC CDR2 and HC CDR3 of a heavy chain variable domain having the amino acid sequence of SEQ ID NO: 42. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, LC CDR2 and LC CDR3 of a light chain variable domain having the amino acid sequence of SEQ ID NO: 43. [000293] In some embodiments, according to the Kabat definition system, the anti-HJV antibody of the present disclosure comprises a HC CDR1 having the amino acid sequence of SEQ ID NO: 1, a HC CDR2 having the amino acid sequence of SEQ ID NO: 2, a HC CDR3 having the amino acid sequence of SEQ ID NO: 12, a LC CDR1 having the amino acid sequence of SEQ ID NO: 15, a LC CDR2 having the amino acid sequence of SEQ ID NO: 23, and a LC CDR3 having the amino acid sequence of SEQ ID NO: 27. [000294] In some embodiments, anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 1, HC CDR2 having the amino acid sequence of SEQ ID NO: 2, and HC CDR3 having the amino acid sequence of SEQ ID NO: 12. “Collectively,” as used anywhere in the present disclosure, means that the total number of amino acid variations in all of the three heavy chain CDRs is within the defined range. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LC CDR2, and a LC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2 or 1 amino acid variation) as compared with the LC CDR1 having the amino acid sequence of SEQ ID NO: 15, LC CDR2 having the amino acid sequence of SEQ ID NO: 23, and LC CDR3 having the amino acid sequence of SEQ ID NO: 27. [000295] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%,at least 96%, at least 97%, at least 98%, or at least 99%) identical to the HC CDR1 having the amino acid sequence of SEQ ID NO: 1, HC CDR2 having the amino acid sequence of SEQ ID NO: 2, and HC CDR3 having the amino acid sequence of SEQ ID NO: 12. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LC CDR2, and a LC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the to the LC CDR1 having the amino acid sequence of SEQ ID NO: 15, LC CDR2 having the amino acid sequence of SEQ ID NO: 23, and LC CDR3 having the amino acid sequence of SEQ ID NO: 27. [000296] In some embodiments, the anti-HJV antibody of the present disclosure comprises: a HC CDR1 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 1; a HC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR2 having the amino acid sequence of SEQ ID NO: 2; and / or a HC CDR3 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR3 having the amino acid sequence of SEQ ID NO: 12. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises: a LC CDR1 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR1 having the amino acid sequence of SEQ ID NO: 15; a LC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR2 having the amino acid sequence of SEQ ID NO: 23; and / or a LC CDR3 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR3 having the amino acid sequence of SEQ ID NO: 27. [000297] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising the amino acid sequence of SEQ ID NO: 42. Alternatively, or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising the amino acid sequence of SEQ ID NO: 43. [000298] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VH as set forth in SEQ ID NO: 42. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acidvariation) as compared with the VL as set forth in SEQ ID NO: 43. In some embodiments, the number of amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) may occur within a VH of SEQ ID NO: 42 and / or a VL of SEQ ID NO: 43 excluding any of the CDR sequences therein. In some embodiments, an anti-HJV antibodies provided herein comprise a heavy chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VH of SEQ ID NO: 42, and / or a light chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VL of SEQ ID NO: 43. [000299] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the VH as set forth in SEQ ID NO: 42. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the VL as set forth in SEQ ID NO: 43. In some embodiments, the degree of sequence variation (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) may occur within a VH of SEQ ID NO: 42, and / or a VL of SEQ ID NO: 43 excluding any of the CDR sequences therein. In some embodiments, an anti-HJV antibody provided herein comprise a heavy chain variable sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VH of SEQ ID NO: 42, and / or a light chain variable sequence that comprises a framework sequence that at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VL of SEQ ID NO: 43. [000300] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, HC CDR2 and HC CDR3 of a heavy chain variable domain having the amino acid sequence of SEQ ID NO: 44. Alternatively or in addition, the anti-HJV antibody of thepresent disclosure comprises a LC CDR1, LC CDR2 and LC CDR3 of a light chain variable domain having the amino acid sequence of SEQ ID NO: 45. [000301] In some embodiments, according to the Kabat definition system, the anti-HJV antibody of the present disclosure comprises a HC CDR1 having the amino acid sequence of SEQ ID NO: 1, a HC CDR2 having the amino acid sequence of SEQ ID NO: 2, a HC CDR3 having the amino acid sequence of SEQ ID NO: 13, a LC CDR1 having the amino acid sequence of SEQ ID NO: 16, a LC CDR2 having the amino acid sequence of SEQ ID NO: 21, and a LC CDR3 having the amino acid sequence of SEQ ID NO: 29. [000302] In some embodiments, anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 1, HC CDR2 having the amino acid sequence of SEQ ID NO: 2, and HC CDR3 having the amino acid sequence of SEQ ID NO: 13. “Collectively,” as used anywhere in the present disclosure, means that the total number of amino acid variations in all of the three heavy chain CDRs is within the defined range. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LC CDR2, and a LC CDR3, which collectively contains no more than 5 amino acid variations (e.g., no more than 5, 4, 3, 2 or 1 amino acid variation) as compared with the LC CDR1 having the amino acid sequence of SEQ ID NO: 16, LC CDR2 having the amino acid sequence of SEQ ID NO: 21, and LC CDR3 having the amino acid sequence of SEQ ID NO: 29. [000303] In some embodiments, the anti-HJV antibody of the present disclosure comprises a HC CDR1, a HC CDR2, and a HC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the HC CDR1 having the amino acid sequence of SEQ ID NO: 1, HC CDR2 having the amino acid sequence of SEQ ID NO: 2, and HC CDR3 having the amino acid sequence of SEQ ID NO: 13. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a LC CDR1, a LC CDR2, and a LC CDR3 that collectively are at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the to the LC CDR1 having the amino acid sequence of SEQ ID NO: 16, LC CDR2 having the amino acid sequence of SEQ ID NO: 21, and LC CDR3 having the amino acid sequence of SEQ ID NO: 29.[000304] In some embodiments, the anti-HJV antibody of the present disclosure comprises: a HC CDR1 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR1 having the amino acid sequence of SEQ ID NO: 1; a HC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR2 having the amino acid sequence of SEQ ID NO: 2; and / or a HC CDR3 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the HC CDR3 having the amino acid sequence of SEQ ID NO: 13. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises: a LC CDR1 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR1 having the amino acid sequence of SEQ ID NO: 16; a LC CDR2 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR2 having the amino acid sequence of SEQ ID NO: 21; and / or a LC CDR3 having no more than 3 amino acid variations (e.g., no more than 3, 2, or 1 amino acid variation) as compared with the LC CDR3 having the amino acid sequence of SEQ ID NO: 29. [000305] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising the amino acid sequence of SEQ ID NO: 44. Alternatively, or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising the amino acid sequence of SEQ ID NO: 45. [000306] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VH as set forth in SEQ ID NO: 44. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL containing no more than 20 amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) as compared with the VL as set forth in SEQ ID NO: 45. In some embodiments, the number of amino acid variations (e.g., no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation) may occur within a VH of SEQ ID NO: 44 and / or a VL of SEQ ID NO: 45 excluding any of the CDR sequences therein. In some embodiments, an anti-HJV antibodies provided herein comprise a heavy chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10, 9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VH of SEQ ID NO: 44, and / or a light chain variable sequence that comprises a framework sequence that that contains no more than 20, 19, 18, 17, 16, 15, 14, 13, 12, 11, 10,9, 8, 7, 6, 5, 4, 3, 2, or 1 amino acid variation to the framework sequence of a VL of SEQ ID NO: 45. [000307] In some embodiments, the anti-HJV antibody of the present disclosure comprises a VH comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the VH as set forth in SEQ ID NO: 44. Alternatively or in addition, the anti-HJV antibody of the present disclosure comprises a VL comprising an amino acid sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, or at least 99%) identical to the VL as set forth in SEQ ID NO: 45. In some embodiments, the degree of sequence variation (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) may occur within a VH of SEQ ID NO: 44, and / or a VL of SEQ ID NO: 45 excluding any of the CDR sequences therein. In some embodiments, an anti-HJV antibody provided herein comprise a heavy chain variable sequence that is at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VH of SEQ ID NO: 44, and / or a light chain variable sequence that comprises a framework sequence that at least 80% (e.g., at least 80%, at least 85%, at least 90%, at least 91%, at least 92%, at least 93%, at least 94%, at least 95%, at least 96%, at least 97%, at least 98%, at least 99%, or 100%) identical to the framework sequence of a VL of SEQ ID NO: 45. [000308] The CDRs of an antibody may have different amino acid sequences when different definition systems are used (e.g., the IMGT definition, the Kabat definition, or the Chothia definition). A definition system annotates each amino acid in a given antibody sequence (e.g., VH or VL sequence) with a number, and numbers corresponding to the heavy chain and light chain CDRs are provided in Table 2. The CDRs listed in Table 1 are defined in accordance with the Kabat definition. One skilled in the art is able to derive the CDR sequences using the different numbering systems for the anti-HJV antibodies provided in Table 1. Table 2. CDR Definitions1IMGT®, the international ImMunoGeneTics information system®, imgt.org, Lefranc, M.-P. et al., Nucleic Acids Res., 27:209-212 (1999)2Kabat et al. (1991) Sequences of Proteins of Immunological Interest, Fifth Edition, U.S. Department of Health and Human Services, NIH Publication No. 91-32423Chothia et al., J. Mol. Biol. 196:901-917 (1987)) [000309] In some embodiments, the anti-HJV antibody of the present disclosure is a chimeric antibody, which can include a heavy constant region and a light constant region from a human antibody. Chimeric antibodies refer to antibodies having a variable region or part of variable region from a first species and a constant region from a second species. Typically, in these chimeric antibodies, the variable region of both light and heavy chains mimics the variable regions of antibodies derived from one species of mammals (e.g., a non-human mammal such as mouse, rabbit, and rat), while the constant portions are homologous to the sequences in antibodies derived from another mammal such as human. In some embodiments, amino acid modifications can be made in the variable region and / or the constant region. [000310] In some embodiments, the anti-HJV antibody described herein is a ...

Claims

CLAIMS What is claimed is:

1. A method of treating myelodysplastic syndrome (MDS) comprising administering an anti-HJV antibody to a functionally iron deficient subject having MDS.

2. A method of treating myelodysplastic syndrome (MDS) comprising administering an anti-HJV antibody to a subject having MDS, wherein the subject has elevated hepcidin levels.

3. The method of claim 1 or 2, wherein the administration results in release of cellular iron stores.

4. The method of any one of claims 1-3, wherein the administration results in release of cellular iron stores in the amount sufficient to treat anemia in the subject.

5. The method of any one of claims 1-4, wherein the subject has low to moderate low MDS according to International Prognostic Scoring System (IPSS) Revised (IPSS-R).

6. The method of any one of claims 1-5, wherein the subject has very low MDS according to International Prognostic Scoring System (IPSS) Molecular (IPSS-M).

7. The method of claim 6, wherein the subject has an IPSS-M risk score of less than - 1.

5.

8. The method of any one of claims 1-5, wherein the subject has low MDS according to IPSS-M.

9. The method of claim 8, wherein the subject has an IPSS-M risk score in the range of - 1.5 to -0.

5.

10. The method of any one of claims 1-5, wherein the subject has moderate low MDS according to IPSS-M.

11. The method of claim 10, wherein the subject has an IPSS-M risk score in the range of -0.5 to 0.

12. The method of any one of claims 1-5, wherein the subject has moderate high MDS according to IPSS-M.

13. The method of claim 12, wherein the subject has an IPSS-M risk score in the range of 0 to 0.

5.

14. The method of any one of claims 1-13, wherein the subject has MDS / myeloproliferative neoplasm (MPN) (MDS / MPN).

15. The method of claim 14, wherein the subject does not have MDS / MPN with ring sideroblasts.

16. The method of claim 14, wherein the MDS / MPN is MDS / MPN with ring sideroblasts and thrombocytosis (RS-T) (MDS / MPN with RS-T).

17. The method of claim 16, wherein the MDS / MPN is chronic myelomonocytic leukemia (CMML).

18. The method of any one of claims 1-13, wherein the subject has Del(5q) MDS.

19. The method of any one of claims 1-13, wherein the subject does not have secondary MDS.

20. The method of any one of claims 1-19, wherein the subject has elevated hepcidin levels.

21. The method of any one of claims 1-20, wherein the is the subject has refractory anemia (RA).

22. The method of any one of claims 1-21, wherein the subject has RA with excess blasts (RAEB).

23. The method of any one of claims 1-22, wherein the subject has RA with ringed sideroblasts (RARS).

24. The method of any one of claims 1-23, wherein the subject has RA with single lineage dysplasia (SLD).

25. The method of any one of claims 1-23, wherein the subject has RA with multilineage dysplasia (MLD).

26. The method of any one of claims 25, wherein the subject has refractory cytopenia with multilineage dysplasia (MLD).

27. The method of any one of claims 1-26, wherein the subject has less than 10% blast cells in the bone marrow.

28. The method of any one of claims 1-27, wherein the subject has 5-10% blast cells in the bone marrow.

29. The method of any one of claims 1-26, wherein the subject has less than 5% blast cells in the bone marrow.

30. The method of any one of claims 1-29, wherein the subject has less than 5% circulating blast cells.

31. The method of any one of claims 1-30, wherein the subject has a baseline hemoglobin level of less than 10 g / dL.

32. The method of any one of claims 1-31, wherein the subject has a baseline serum ferritin level of at least 30 µg / L.

33. The method of any one of claims 1-32, wherein the subject has a baseline platelet count in the range of 25,000-1,000,000 / µL.

34. The method of any one of claims 1-33, wherein the subject has a baseline total white blood cell count of less than 50,000 / µL.

35. The method of any one of claims 1-34, wherein the subject has a transferrin saturation (TSAT) level of less than 75%.

36. The method of any one of claims 1-35, wherein the subject has a baseline level of aspartate aminotransferase (AST) of less than 3.0x upper limit of normal (ULN).

37. The method of any one of claims 1-36, wherein the subject has a baseline level of alanine transaminase (ALT) of <3.0x ULN.

38. The method of any one of claims 1-37, wherein the subject has a baseline level of direct bilirubin of <2.0x ULN.

39. The method of any one of claims 1-38, wherein the subject has an estimated glomerular filtration rate (eGFR) of at least 30mL / min / 1.73m2.

40. The method of any one of claims 1-39, wherein the subject has an Eastern Cooperative Oncology Group (ECOG) performance score of less than 2.

41. The method of any one of claims 1-40, wherein the subject comprises one or more mutations in TET2, ASXL1, NRAS, JAK2, CBL, IDH2, NPM1, IDH1, KRAS, GNAS, PTPN11, BRAF, PTEN, and / or CDKN2A.

42. The method of any one of claims 1-41, wherein the subject does not have neutropenia.

43. The method of any one of claims 1-42, wherein the subject does not have thrombocytopenia.

44. The method of any one of claims 1-43, wherein the subject does have acute myeloid leukemia (AML).

45. The method of any one of claims 1-44, wherein the subject does not have vitamin B12 deficiency.

46. The method of any one of claims 1-45, wherein the subject does not have folate deficiency.

47. The method of any one of claims 1-46, wherein the subject does not have an infection.

48. The method of any one of claims 1-47, wherein the subject does not have hereditary hemochromatosis.

49. The method of any one of claims 1-48, wherein the subject does not have a hemoglobinopathy associated with anemia.

50. The method of any one of claims 1-49, wherein the subject does not have an intrinsic red blood cell defect associated with anemia.

51. The method of any one of claims 1-50, wherein the subject does not have active immune-mediated hemolytic anemia.

52. The method of any one of claims 1-51, wherein the subject does not have non-surgical bleeding causing a decrease in hemoglobin of more than 2g / dL.

53. The method of any one of claims 1-52, wherein the subject has received no more than 2 units of red blood cell transfusion 6 months prior to administration of the anti-HJV antibody to the subject.

54. The method of any one of claims 1-53, wherein the subject has received no more than 12 units of red blood cell transfusion for MDS related anemia.

55. The method of any one of claims 1-54, wherein the subject has not received a hematopoietic cell transplant within 10 years of the administration of the anti-HJV antibody.

56. The method of any one of claims 1-55, wherein the subject has not received iron chelation therapy within 28 days of the administration of the anti-HJV antibody.

57. The method of any one of claims 1-56, wherein the subject has not received a total splenectomy.

58. The method of any one of claims 1-57, wherein the subject has not received major surgery within 8 weeks of the administration of the anti-HJV antibody.

59. The method of any one of claims 1-58, wherein the subject has not been diagnosed with a malignancy within 3 years of the administration of the anti-HJV antibody to the subject.

60. The method of any one of claims 1-59, wherein the subject has not received anemia directed therapies within 28 days of the administration of the anti-HJV antibody.

61. The method of any one of claims 1-60, wherein the subject has received MDS treatment prior to the administration of the anti-HJV antibody.

62. The method of any one of claims 1-61, further comprising administering a therapeutic agent for treating MDS to the subject.

63. The method of claim 62, wherein the anti-HJV antibody and the therapeutic agent for treating MDS are administered concomitantly, or sequentially.

64. The method of claim 62, wherein the anti-HJV antibody and the therapeutic agent for treating MDS are administered at different frequencies.

65. The method of any one of claims 62-64, wherein the therapeutic agent for treating MDS is for iron chelation.

66. The method of any one of claims 62-65, wherein the therapeutic agent for treating MDS isa growth factor.

67. The method of any one of claims 62-66, wherein the therapeutic agent for treating MDS is luspatercept.

68. The method of any one of claims 62-67, wherein the therapeutic agent for treating MDS is lenalidomide.

69. The method of any one of claims 62-68, wherein the therapeutic agent for treating MDS is an immune modulator.

70. The method of any one of claims 62-69, wherein the therapeutic agent for treating MDS is allogeneic stem cell transplantation.

71. The method of any one of claims 62-70, wherein the therapeutic agent for treating MDS a hypomethylating agent (HMA).

72. The method of any one of claims 1-71, wherein the anti-HJV antibody is administered intravenously or subcutaneously.

73. The method of any one of claims 1-72, wherein the antibody comprises a HC CDR1 comprising the amino acid of SEQ ID NO: 1, a HC CDR2 comprising the amino acid of SEQ ID NO: 2, a HC CDR3 comprising the amino acid of SEQ ID NO: 3; an LC CDR1 comprising the amino acid of SEQ ID NO: 17, a LC CDR2 comprising the amino acid of SEQ ID NO: 5, and a LC CDR3 comprising the amino acid of SEQ ID NO:

27.

74. The method of any one of claims 1-73, wherein the anti-HJV antibody comprises a VH comprising the amino acid sequence of SEQ ID NO: 38, and a VL comprising the amino acid sequence of SEQ ID NO:

39.

75. The method of any one of claims 1-74, wherein the anti-HJV antibody comprises a heavy chain comprising the amino acid sequence of SEQ ID NO: 61, and a light chain comprising the amino acid sequence of SEQ ID NO: 62.

76. The method of any one of claims 1-74, wherein the anti-HJV antibody comprises a heavy chain comprising the amino acid sequence of SEQ ID NO: 63, and a light chain comprising the amino acid sequence of SEQ ID NO:

62.

77. The method of any one of claims 1-76, wherein the administration of an anti-HJV antibody increases hemoglobin level in the subject.

78. The method of any one of claims 1-77, wherein the administration of an anti-HJV antibody increases hemoglobin level in the subject by at least 1 g / dL.

79. The method of any one of claims 1-78, wherein the administration of an anti-HJV antibody increases TSAT% in the subject relative to the TSAT% prior to administration.

80. The method of any one of claims 1-79, wherein the administration of an anti-HJV antibody increases TSAT% in the subject by between 10% and 50%, between 10% and 40%, between 10% and 30%, between 10% and 20%, or between 10% and 15%, relative to the TSAT% prior to administration.

81. The method of any one of claims 1-80, wherein the administration of an anti-HJV antibody decreases circulating hepcidin level in the subject relative to the circulating hepcidin level prior to administration.

82. The method of any one of claims 1-81, wherein the administration of an anti-HJV antibody decreases circulating hepcidin level in the subject by between 5% and 30%, between 5% and 20%, or between 5% and 15%, relative to the circulating hepcidin level prior to administration.

83. The method of any one of claims 1-82, wherein the administration of an anti-HJV antibody increases serum iron level in the subject compared to before administration.

84. The method of any one of claims 1-83, wherein the administration of an anti-HJV antibody increases mean corpuscular hemoglobin in the subject compared to before administration.

85. The method of any one of claims 1-83, wherein the administration of an anti-HJV antibody increases mean corpuscular hemoglobin concentration in the subject compared to before administration.

86. A method for treating anemia in a subject having a myelodysplastic syndrome (MDS), the method comprising administering an effective amount of an anti-hemojuvelin (HJV) antibody to the subject.

87. A method for treating functional iron deficiency (FID) in a subject having a myelodysplastic syndrome (MDS), the method comprising administering an effective amount of an anti-hemojuvelin (HJV) antibody to the subject.

88. A method for treating very low to moderate low myelodysplastic syndrome (MDS) in a subject, the method comprising administering an effective amount of an anti-hemojuvelin (HJV) antibody to the subject.

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