306 results about "Host disease" patented technology

The present disclosure relates to mesenchymal lineage precursor or stem cell mediated methods for treating severe Graft versus Host Disease (GvHD) in subjects at high risk of poor outcomes.

The purpose of the present invention is to provide a novel therapeutic agent or prophylactic agent for dry eye, a therapeutic agent or prophylactic agent for a graft-versus-host disease, a corneal epithelial wound healing promoter, an inflammatory cell inhibitor that infiltrates the cornea, a tear fluid amount retaining agent, a corneal epithelial disorder inhibitor, a cell proliferation marker-positive cell inhibitor, and an inhibitor of lymphocyte differentiation into effector T cells. The present invention provides the following, each of which contains, as an active ingredient, a substance derived from a culture supernatant of stem cells: a therapeutic agent or prophylactic agent for dry eye; a therapeutic agent or prophylactic agent for a graft-versus-host disease; a corneal epithelial wound healing promoter; an inflammatory cell inhibitor infiltrating into the cornea; a tear fluid amount retaining agent; a corneal epithelial disorder inhibitor; a cell proliferation marker-positive cell inhibitor; or an inhibitor of lymphocyte differentiation into effector T cells.

Disclosed are methods of treating patients receiving an organ transplant by administering extracellular vesicle composition.

The purpose of the present invention is to provide: a novel therapeutic or prophylactic agent for xerophthalmia; a therapeutic or prophylactic agent for graft-versus-host disease; a corneal epithelium wound healing promoter; a corneal invasive inflammatory cell inhibitor; or an inhibitor of differentiation of lymphocytes into effector T cells. The present invention provides: a therapeutic or prophylactic agent for xerophthalmia, a therapeutic or prophylactic agent for graft-versus-host disease, a corneal epithelial wound healing promoter, a corneal invasive inflammatory cell inhibitor, a tear amount maintenance agent, a corneal epithelial damage inhibitor, and a method for preparing the same, which comprises, as an active ingredient, a substance derived from a stem cell culture supernatant; a cell proliferation marker positive cell inhibitor, or an inhibitor of differentiation of lymphocytes to effector T cells.

The invention provides a method for enhancing Treg cell functions and application, and belongs to the technical field of cell engineering. According to the method, hUC-MSCs are irradiated by gamma rays to form feeder layer cells, and then the feeder layer cells and Treg cells are co-cultured to obtain the Treg cells with enhanced cell functions. Through the co-culture of the feeder layer cells and the Treg cells, the inhibition ability of the Treg cells on activation and proliferation of immune cells can be enhanced, and the feeder layer cells and the Treg cells can be used as universal cells in clinical researches of autoimmune diseases, graft versus host diseases and the like.

A fibroblast activation protein (FAP) targeting chimeric antigen receptor macrophage and its construction method and application. The expression of FAP increases in senescent cells of various senescent diseases. Immune cells, especially macrophages, specifically eliminates senescent cells after expressing chimeric antigen receptor recognizing FAP protein, thereby reducing the pathogenic effect of senescent cells. Macrophages expressing the FAP chimeric antigen receptor can undergo M2-type polarization, which do not produce inflammatory factors to deteriorate age related diseases, have good infiltration ability to tissues with dense matrix, do not induce graft-versus-host disease and have high recognition efficiency of senescent cells and good phagocytic effect. This provides a new idea for preparing reagents for eliminating senescent cells, which have wide potential in practical application.

The invention provides sgRNA for targeting and guiding nuclease to efficiently cut an HLA-DRA gene, a method for modifying a CAR-T cell by using the sgRNA, and a related gene editing system, reagent and kit. According to the CAR-T cell, the immunogenicity is greatly reduced, the risk of graft versus host disease and immunological rejection can be effectively reduced, and meanwhile the killing capacity of tumor cells of the CAR-T cell is not affected.

Disclosed herein are methods of treating a disease selected from graft-versus-host disease (GVHD), systemic sclerosis (scleroderma), chronic lung allograft dysfunction (CLAD), restrictive allograft syndrome (RAS), and bronchiolitis obliterans syndrome (BOS) using a combination of a BTK inhibitor (such as rilzabrutinib) and belumosudil.

The present invention relates to double stranded oligonucleotides that are complementary to JAK1, leading to modulation of the expression of JAK1. Modulation of JAK1 expression is beneficial for a range of medical disorders including inflammatory bowel disease, organ transplant rejection, graft-versus-host disease, multiple sclerosis, rheumatoid arthritis (RA), juvenile idiopathic arthritis, psoriasis, dermatitis, diabetic nephropathy, systemic lupus erythematosus (SLE), dry eye disease, cancer, myelofibrosis, and asthma. Also included are compositions comprising the double stranded oligonucleotide and methods of treatment using the double stranded oligonucleotide.

This disclosure relates to methods of using an anti-CD26 antibody and antigen binding fragments thereof for the treat-ment of graft versus host disease.

The invention provides agonistic TNFR2 antibodies and antigen-binding fragments thereof and encompasses the use of these antibodies as therapeutics to promote the proliferation of regulatory T cells (T-reg) for the treatment of immunological diseases. Antibodies of the invention can be used to potentiate the T-reg-mediated deactivation of self- and allergen-reactive T- and B-lymphocytes, and can thus be used to treat a wide variety of indications, including autoimmune diseases, allergic reactions, asthma, graft-versus-host disease, and allograft rejection, among others.

The present invention relates to high density lipoprotein (HDL) or HDL mimetics for use in the prevention and / or treatment of graft-versus-host disease (GvHD) or cytokine release syndrome in a subject.

Isolated anti-human CD45RC antibodies or binding fragments thereof, nucleic acids and expression vector encoding the same, compositions including the same, and uses thereof as medicaments, including for the prevention and / or treatment of CD45RChigh-related diseases (including autoimmune diseases, undesired immune responses, monogenic diseases, and lymphoma or cancer), in particular for use in preventing and / or treating graft-versus-host disease (GVHD).

The invention relates to bispecific antibodies comprising a first antigen-binding domain that specifically binds to TfR and a second, and optionally a third, antigen-binding domain that specifically binds to PD1. The invention further relates to methods of producing these molecules, to methods of using the same, to pharmaceutical compositions thereof, and their use as medicaments for the treatment of cancer, of acute and chronic infections and of Graft-versus-host disease.

A method for treating or preventing GvHD in a human patient, comprising administering to a patient suffering from GvHD or at risk for GvHD, a humanized antibody having binding specificity for human α4β7 integrin, wherein the human patient has or is going to have an allogeneic stem cell transplantation, and wherein the dosing regimen prevents, improves or eliminates GvHD.

The present invention relates to the field of biomedicine, and in particular to the use of Mycobacterium finschii in the preparation of a drug for treating acute graft-versus-host disease. The present invention clarifies a specific strain of Mycobacterium finschii that has the effect of inhibiting acute graft-versus-host disease. By obtaining a single strain of bacteria with an inhibitory effect, it is helpful to prepare drugs in a standardized and streamlined manner, thereby obtaining drugs with clear ingredients, strict quality testing, and direct clinical application, so that the same standard drug can be widely used in patients with acute graft-versus-host disease, thereby improving the universality of the drug.

This invention provides an antibody composition with improved stability, exhibiting reduced fragmentation of the antibody polypeptide chain during manufacturing and subsequent storage. [Solution] This disclosure relates to improved compositions and methods for treating T cell-mediated diseases and disorders (e.g., autoimmune disorders, graft-versus-host diseases, and graft rejection). Provided are antibody-containing anti-αβTCR binding polypeptides comprising at least one amino acid substitution or modification that enhances the stability of the binding polypeptide by reducing fragmentation of the light chain variable region. Methods provided herein generally involve administering an effective amount of a stabilized, humanized binding polypeptide specific to the alpha-beta T cell receptor (αβTCR) to a subject in need thereof.

The present application relates to interleukin-2 variants and methods of use thereof. The present invention relates to polypeptides that share a primary sequence with human IL-2 in addition to several mutated amino acids. A panel of IL-2 variants comprises mutations with profound impressive manufacturability that preferentially promote proliferation, survival, activation and / or function of immunosuppressive regulatory T cells (Treg: CD4 + CD25 + FoxP3 +) over effector T cells and NK cells. Also included is the therapeutic use of such IL-2 selective agents, alone or in combination with immunomodulators or disease tissue targeting antibodies, proteins or peptides, for the treatment of Treg cell deficiency, various autoimmune and inflammatory disorders, organ transplantation and graft versus host disease. In another aspect, the invention relates to pharmaceutical compositions comprising the disclosed polypeptides. Finally, the invention relates to the therapeutic use of the disclosed polypeptides and pharmaceutical compositions due to their selective modulation of the immune system on diseases such as autoimmune and inflammatory disorders.

This disclosure relates to an immunoglobulin single variable domain (ISVD)-containing modulator that allosterically binds to a three-dimensional (3D) epitope of a protein complex comprising at least one inhibitory immune receptor and at least one corresponding ligand. The modulator regulates cooperativity within such complexes, thereby affecting the binding affinity and downstream signaling pathways. Specifically, the allosteric modulator of this invention induces positive cooperativity in immunoinhibitory receptor-ligand complexes, thus suppressing immune responses in a spatiotemporally restricted manner. Accordingly, these allosteric modulators are useful as therapeutic agents for inflammatory diseases, such as autoimmune diseases, allergic diseases, or graft-versus-host disease (GVHD). Moreover, this disclosure pertains to methods for identifying, selecting, and producing said allosteric modulators.

The present invention provides a method of reducing the likelihood of a subject having graft versus host disease or a method of treating graft versus host disease in a subject comprising analyzing a gastrointestinal biopsy of the subject to measure the number and density proportion of cells and administering to the subject a pharmaceutically effective amount of one or more immunosuppressive agents.

The present disclosure relates to mesenchymal lineage precursor or stem cell mediated methods for treating severe Graft versus Host Disease (GvHD) in subjects that are refractory to at least two prior lines of therapy.

The present invention provides a prophylactic or therapeutic composition for graft-versus-host disease (GVHD). There is provided a prophylactic or therapeutic composition for GVHD, which comprises bacteria belonging to any genus selected from the group consisting of the following genera: Blautia, Clostridium, unclassified Clostridiales, Actinomyces, Parabacteroides, Lachnoclostridium, Bacteroides, Faecalibacterium, unclassified Lachnospiraceae, Roseburia, Ruminococcus, unclassified Firmicutes, Dorea, Phascolarctobacterium, Sutterella, Megamonas, Collinsella, Eubacterium, and Coprococcus, etc., or any combination of bacteria belonging to these genera.

The present invention provides a liposome preparation containing a population of liposomes containing a CD1d ligand compound, wherein the average particle size of the population of liposomes is 90 to 110 nm and the polydispersity index of particle size distribution is 0.2 or less. and the polydispersity index of the particle size distribution is 0.2 or less. The present invention also provides the use of the liposome preparation in the prevention or treatment of graft-versus-host disease and organ transplant rejection.

The application discloses a method for establishing a mouse model of MHC haplotype compatible allogeneic hematopoietic cell transplantation, and belongs to the technical field of animal experiment model construction. The technical problem to be solved by the application is how to construct a mouse model which can be used to study the immune reconstruction mechanism and treatment effect evaluation of MHC haplotype compatibility and MHC full compatibility in bone marrow cell transplantation recipient mice. To solve the technical problem, the application provides a method for constructing a mouse model of MHC haplotype compatible allogeneic hematopoietic cell transplantation, which comprises transplanting bone marrow cells of a donor mouse into a recipient mouse, and the MHC haplotype of the donor mouse and the recipient mouse is compatible. The application sets a modeling condition, and the model establishment condition is evaluated by survival condition, graft-versus-host disease and rejection reaction observation, flow cytometry and histopathological section, so as to prove that the model is reliable and stable.

The present invention provides a novel use and methods comprising antibodies, or antigen-binding fragments thereof, which bind to a CCR7 receptor for use as a novel therapeutic agent in prevention and / or treatment of graft versus host disease (GVHD), preferably in hematopoietic stem cell transplantation (HSCT), more preferably allogeneic hematopoietic stem cell transplantation. GVHD of the invention can be acute (aGVHD) and / or chronic (cGVHD), preferably acute. The antibodies and antigen-binding fragments are capable of selectively depleting ex vivo or in vitro immune cells expressing CCR7 and are capable in vivo of selectively killing immune cells expressing a CCR7 receptor and of impairing / blocking migration and of activation of said immune cells, which are involved in the development and evolution of GVHD. The use of said antibodies for depleting, killing and impairing / blocking migration and activation of immune cells expressing CCR7 cells is disclosed, thus providing an alternative therapy for preventing and treating GVHD in both acute and chronic types.

The present disclosure provides a scalable and practical off-the-shelf allogeneic T cell therapy for treating cancer including employing a population of nonexhausted allogeneic virus specific CD4+ T cells, CD8+ T cells or CD4+ and CD8+ T cells that express a nonexhausted PD-1negTIGITnegTCF-1High TOXLo early stem cell TSCM phenotype. The virus-specific population of CD4+ T cells, CD8+ T cells or CD4+ and CD8+ T cells that expresses the nonexhausted early stem cell TSCM phenotype and comprises TCRs specific for a protein of a virus is genetically modified to stably express up to three chimeric antigen-receptors (CARs). Each CAR is specific for a cancer antigen. At least one of the CARs comprises a CD30 CAR expressing a CD30-specific scFv fragment, and / or a chimeric alloimmune defense receptor (ADR); and / or a chimeric HLA accessory receptor fused with a cytolytic endodomain of the T cell receptor zeta chain, thereby reducing risk of host versus graft rejection (HVGR). In some regimens, multiple populations of cells can be combined and co-infused as the off the shelf T cell therapies.

This invention relates to double-stranded oligonucleotides complementary to JAK1 that result in the regulation of JAK1 expression. Regulation of JAK1 expression is beneficial for a range of medical disorders, including inflammatory bowel disease, organ transplant rejection, graft-versus-host disease, multiple sclerosis, rheumatoid arthritis (RA), juvenile idiopathic arthritis, psoriasis, dermatitis, diabetic nephropathy, systemic lupus erythematosus (SLE), dry eye disease, cancer, myelofibrosis, and asthma. The invention also includes compositions comprising double-stranded oligonucleotides and therapeutic methods using double-stranded oligonucleotides.

The present invention relates to a compound of Formula (I), in particular, the compound of Formula (II) or an isotopic variant, a pharmaceutically acceptable salt or solvate thereof for use in a method of treatment of graft-versus-host disease in a subject in need thereof.

The present application belongs to the field of photochemical therapy, and particularly relates to a method for photochemical treatment of riboflavin based on multi-wavelength LED and application thereof in treatment of graft-versus-host disease. The present application selects different wavelength LED combinations as light sources to optimize the riboflavin photochemical method, controls the light intensity at 1000-25000 μW / cm², controls the irradiation time at 5-15 minutes, and controls the riboflavin concentration at 20-150 μM, thereby significantly improving the photochemical reaction effect. The method can efficiently induce PBMC apoptosis in a plasma environment, significantly reduces the levels of key pro-inflammatory cytokines such as TNF-α, IL-6 and IFN-γ, and has no significant influence on platelets, hemoglobin and blood clotting function, thereby providing a safe and controllable new cell preparation method for GVHD treatment.

A method for treating subjects with graft-versus-host disease (GvHD) or at risk of developing GvHD, using CD90 with stronger immunomodulatory capabilities. + hAEC cell populations were used as the primary therapeutic cells. Studies on the related mechanism of action revealed that CD90... + hAECs showed significantly higher levels of stem cell pluripotency markers SSEA4, OCT4, and NANOG than typical hAECs, and also exhibited better immunomodulatory functions; therefore, CD90 was used as a marker. + hAECs cells can be used as a treatment to achieve better clinical outcomes.