20 results about "CD52" patented technology

The present invention relates to thermostable and thermoactive monoclonal antibodies, or antigen-binding fragments thereof, that have binding specificity to CD52g. The invention also relates to the production of such monoclonal antibodies and their use as contraceptive agents.

The present invention relates to methods for developing engineered T-cells for immunotherapy that are both non-alloreactive and resistant to immunosuppressive drugs. The present invention relates to methods for modifying T-cells by inactivating both genes encoding target for an immunosuppressive agent and T-cell receptor, in particular genes encoding CD52 and TCR. This method involves the use of specific rare cutting endonucleases, in particular TALE-nucleases (TAL effector endonuclease) and polynucleotides encoding such polypeptides, to precisely target a selection of key genes in T-cells, which are available from donors or from culture of primary cells. The invention opens the way to standard and affordable adoptive immunotherapy strategies for treating cancer and viral infections.

The application discloses application of CD52 protein in preparation of a medicine for treating recurrent spontaneous abortion, and belongs to the technical field of biological medicine. It is found that the CD52 protein can target and inhibit abnormal activation of effector T cells at a maternal-fetal interface, reduce release of proinflammatory factors (such as IFN-gamma), thereby reversing immune tolerance imbalance and improving pregnancy outcome. The CD52 protein is applied to the treatment of recurrent spontaneous abortion for the first time, and has the advantages of high targeting and high safety.

The present invention provides a cell surface marker for differentiating a new subset of lineage-biased human multipotent progenitor cells and its application. The cell surface marker is CD52. The new subset of lineage-biased human multipotent progenitor cells is divided into MPP1 subset and MPP2 subset by using the surface marker CD52. The MPP1 subset is CD52+MPP, which tends to differentiate into the lymphoid and myeloid lineages during hematopoietic cell lineage differentiation. The MPP2 subset is CD52−MPP, which tends to differentiate into the erythroid and megakaryocytic lineages during hematopoietic cell lineage differentiation. The surface marker can highly enrich myeloid-lymphoid progenitor cells and erythroid-megakaryocytic progenitor cells, thereby significantly improving the efficiency of directed induction of umbilical cord blood cells into specific blood cell products such as red blood cells, megakaryocytes, neutrophils, NK cells, T cells, B cells, etc., providing an important basis for studying the lineage differentiation of human hematopoietic stem and progenitor cells and clinical applications.

Provided herein are CD70-binding proteins comprising a CD70-binding domain and a transmembrane domain, engineered immune cells comprising the CD70-binding proteins, and methods of making and using the same. Also provided herein are engineered immune cells e.g. CAR (chimeric antigen receptor) T cells for administration to patients to treat cancer (e.g., solid tumors and hematologic tumors) and other unwanted conditions. The cells are engineered to functionally express a first antigen binding molecule e.g. a CD70 CAR and a second antigen binding molecule e.g. a second CAR that binds a target molecule characteristic of the cancer or other disease or unwanted condition. The cells may be further engineered to reduce the functional expression level of one or more of TRAC, CD52 and CD70. Also provided are methods of making and using the engineered cells, compositions and kits comprising them, and methods of treating by administering them.

The present application relates to the technical field of extracellular vesicle sorting, and particularly relates to a epididymal body specific sorting marker, and an epididymal body sorting kit and method. The present application finds that CD52 can be used as a specific marker for sorting epididymal bodies. The present application is the first time to directly separate epididymal bodies from human seminal plasma, the sample is easy to obtain, and the operation process is non-invasive, safe, and the separation path is simple and easy to operate. In addition, it provides a method for the separation of other tissue-specific EV subpopulations. The present application can contribute to further explore the effect of epididymal bodies on sperm function and improve sperm function, and epididymal bodies as a marker have great potential for clinical diagnosis and treatment.

To provide genetically modified immune cells having enhanced anti-neoplasia activity, resistance to immune suppression, and decreased risk of eliciting a graft versus host reaction, or a combination thereof.SOLUTION: Provided is a composition comprising two or more immune cells, each immune cell comprising a) a different chimeric antigen receptor that targets an antigen selected from the group consisting of CD5, CD7, CD3, CD33, and CD123, wherein the immune cells comprise mutations that reduce or eliminate expression of the targeted antigens; and b) one or more mutations that reduce or eliminate the expression of an immunogenic polypeptide selected from the group consisting of TRAC, LAG-3, FAS, CIITA, TRBC1, TRBC2, CD52, B2M, and PD1.SELECTED DRAWING: None

The invention discloses application of CD52 protein in preparation of a medicine for treating recurrent abortion, and belongs to the technical field of biological medicine. It is found that the CD52 protein can inhibit abnormal activation of maternal-fetal interfacial effect T cells in a targeted mode and reduce release of proinflammatory factors (such as IFN-gamma), so that immune tolerance imbalance is reversed, and the pregnancy outcome is improved. The CD52 protein is applied to treatment of the recurrent abortion for the first time, and the CD52 protein has the advantages of being high in targeting performance and high in safety.

The present invention relates to the field of diagnostics and therapeutics against leukemia. More specifically, it relates to a method for assessing acute myeloid leukemia (AML) in a subject suspected to suffer therefrom comprising the steps of determining in a sample of said subject the amount of at least one biomarker selected from the group consisting of: CLEC7A, CLEC9A, HCST, LST1, LTB, IFITM3, CD74, HLA-DRA, CD164, CD52, CD34, HSPA5, MGST1, CD47, TFPI, IGHM, SELL, CD82, CD69, NDFIP1, RALA, RAB11A, SELENOK, HLA- DRB5, RAMP1, IGLL1, HLA-DQA1, CD96, SLC5A3, VAMPS, CALCRL, LPAR6, NINJ1, CD7, SLC2A5, EREG, FCMR, DLK1, and J AML,, comparing the said amount of the at least one biomarker to a reference, and assessing AML based on the comparison. Yet, the present invention relates to a method for generating a bispecific binding agent and to the use of such bispecific binding agents for treating leukemia, preferably, AML.

This invention relates to the diagnosis and evaluation of juvenile myelomonocytic leukemia (JMML). In particular, the invention relates to a method for diagnosing JMML in a subject, comprising: a) at least one biomarker present on or in hematopoietic stem cells and progenitor cells (HSPCs) in a biological sample, i) CD52, RAMP1, LTB, LST1, JAML, IFITM3, CD7, CD69, CD164, CD74, TNF, TFPI, DLK1, CD82, IGHM, CALCRL, RALA, SLC2A5, HSPA5, HLA-DRA, RAB11A, SELL, VAMP5, FCMR, CLEC7A, NDFIP The present invention relates to a method comprising the steps of: 1) determining the amount of at least one biomarker selected from each of the following groups: 1) Group I consisting of CLEC9A, HCST, LPAR6, HLA-DQA1, HLA-DRB5, and CD34; and 2) Group II consisting of IGLL1, BEST1, EREG, SLC5A3, SERK, PRRG3, NINJ1, MGST1, and HLA-G; b) comparing the determined amount in step a) with a reference; and c) diagnosing JMML based on the comparison in step b). Furthermore, the present invention relates to a method for classifying subjects suffering from JMML into a low- or high-risk JMML group. Furthermore, the present invention relates to the use of at least one biomarker present on or in HSPC in a biological sample for diagnosing JMML to a low- or high-risk JMML group in subjects who have JMML or are at risk of developing it. Furthermore, the present invention relates to a kit for diagnosing JMML in a subject or for classifying a subject suffering from JMML into a low- or high-risk JMML group.Furthermore, the present invention relates to an inhibitor for use in the treatment and / or prevention of JMML that specifically inhibits at least one biomarker selected from the group consisting of CD52, RAMP1, LTB, LST1, JAML, IFITM3, CD7, CD69, CD164, CD74, TNF, TFPI, DLK1, CD82, IGHM, CALCRL, RALA, SLC2A5, HSPA5, HLA-DRA, RAB11A, SELL, VAMP5, FCMR, CLEC7A, NDFIP1, CLEC9A, HCST, LPAR6, HLA-DQA1, HLA-DRB5, CD34, IGLL1, BEST1, EREG, SLC5A3, SELK, PRRG3, NINJ1, MGST1, and HLA-G, which are present on or in hematopoietic stem cells and progenitor cells (HSPCs). The present invention further relates to a pharmaceutical composition for use in the treatment and / or prevention of JMML, comprising at least two inhibitors according to the present invention. Finally, the present invention envisions a method for treating and / or preventing JMML.

Provided herein are CD70-binding proteins comprising a CD70-binding domain and a transmembrane domain, engineered immune cells comprising the CD70-binding proteins, and methods of making and using the same. Also provided herein are engineered immune cells e.g. CAR (chimeric antigen receptor) T cells for administration to patients to treat cancer (e.g., solid tumors and hematologic tumors) and other unwanted conditions. The cells are engineered to functionally express a first antigen binding molecule e.g. a CD70 CAR and a second antigen binding molecule e.g. a second CAR that binds a target molecule characteristic of the cancer or other disease or unwanted condition. The cells may be further engineered to reduce the functional expression level of one or more of TRAC, CD52 and CD70. Also provided are methods of making and using the engineered cells, compositions and kits comprising them, and methods of treating by administering them.

The invention provides exosome miRNA closely related to SLE, a target gene and application of the exosome miRNA and the target gene, and belongs to the technical field of biological medicine. The exosome miRNA is let-7f-5p, and the RNA sequence table of the exosome miRNA is as shown in SEQ ID No. 1. The target genes of the exosome miRNA closely related to the SLE comprise Cd52, Gbp2, Gbp7 and Gatm, and the amino acid sequences of the coding proteins of the target genes are respectively shown as SEQ ID No.2-5. According to transcriptomic analysis, the biological function of an abnormally expressed gene is matched with that of an SLE related signal channel, let-7f-5p is abnormally expressed in lupus nephritis, and the exosome miRNA can be used as a biomarker for clinical diagnosis of SLE. The let-7f-5p can relieve the inflammatory state of an RAW264.7 cell inflammation model, and mesenchymal stem cell co-culture can relieve the inflammatory state of macrophages, so that the expression of the let-7f-5p in the macrophage inflammation model is increased, and the expression of a target gene Gbp7 of the let-7f-5p in the macrophage inflammation model is reduced, and further verification shows that the let-7f-5p can be used as the SLE biomarker.

The present invention relates to the diagnosis and assessment of juvenile granulocytic leukemia (JMML). In particular, it relates to a method of diagnosing JMML in a subject, said method comprising: a) determining the amount of at least one biomarker present on or in hematopoietic stem and progenitor cells (HSPC) in a biological sample, said at least one biomarker being selected from the group consisting of i) Group I consisting of CD52, RAMP1, LTB, LST1, JAML, IFITM3, CD7, CD69, CD164, CD74, TNF, TFPI, DLK1, CD82, IGHM, CALCRL, RALA, SLC2A5, HSPA5, HLA-DRA, RABI1A, SELL, VAMPS, FCMR, CLEC7A, NDFIP1, CLEC9A, HCST, b) comparing the quantity determined in step a) with a reference; and c) diagnosing the JMML based on the comparison of step b). In addition, the invention also relates to a method for classifying subjects suffering from JMML as a low-risk or high-risk group of JMML. Furthermore, the invention relates to the use of at least one biomarker present on or in HSPC in a biological sample for diagnosing JMML in a subject suffering from or at risk of developing into JMML as a low-risk or high-risk group of JMML. Furthermore, the present invention relates to a kit for diagnosing JMML in a subject or classifying a subject suffering from JMML as a low-risk group or a high-risk group of JMML. Furthermore, the present invention relates to the use of an inhibitor for the treatment and / or prevention of JMML, said inhibitor specifically inhibiting at least one biomarker selected from the group consisting of CD52, RAMP1, LTB, LST1, JAML, IFITM3, CD7, CD69, CD164, CD74, TNF, TFPI, DLK1, CD82, IGHM, CALCRL, RALA, SLC2A5, HSPA5, HLA-DRA, RABI1A, SELL, VAMPS, FCMR, CLEC7A, NDFIP1, CLEC9A, HCST, LPAR6, HLA-DQA1, HLA-DRB5, CD34, IGLL1, B, present on or in hematopoietic The invention also relates to a pharmaceutical composition for the treatment and / or prevention of JMML, said pharmaceutical composition comprising at least two inhibitors according to the invention. Finally, the present invention envisages a method of treating and / or preventing JMML.

The present invention relates to three different functional heterogeneous megakaryocyte subpopulations that may exist in mouse megakaryocytes (MK), and the specific molecular markers of these subpopulations are identified respectively, including MYLK4, a MK molecular marker that serves as a microenvironment support cell of HSC; LSP1, CD53 or CD52, a MK molecular marker that performs an immunomodulatory function; and ARNTL, a MK molecular marker that has a plate production function. These molecular markers can be used to separate or mark MKs with different functions, thereby promoting MKs to perform different functions, including supporting HSC quiescence, immunomodulation, plate production, etc.

The invention relates to an amplification method of natural killer cells, and belongs to the technical field of cell amplification. The amplification method comprises the following steps: S1, pre-coating a culture container with a monoclonal antibody combination, wherein the monoclonal antibody combination comprises CD56 or CD16, NKG2D and CD52; s2, inoculating umbilical cord blood or peripheral blood mononuclear cells into the pre-coated culture container, and culturing by adopting an activation culture medium containing cytokines to obtain activated cells; s3, transferring the activated cells into a serum-free amplification culture medium containing IL-2 and albumin for amplification culture; and S4, collecting the cells, regulating the cells to the density of 5 * 10 <-15 > * 10 / mL by using a solution containing albumin, standing for 0.5-1.5 hours, and filtering to obtain the natural killer cells. According to the amplification method, the in-vitro amplification multiple of the NK cells and the tumor killing efficiency can be improved.

The present disclosure relates to the use of cells having discernible surface protein with engineered or naturally occurring mutation(s) but functional surface protein for use in therapy. The present invention also relates to the use of cells having discernible CD52 surface protein variants but functional surface protein for use in therapy, in particular adoptive cell therapy.

Multi-specific binding proteins that binds NKG2D receptor, CD 16, and a tumor-associated antigen selected from CD37, CD20, CD19, CD22, CD30, CD52, and CD133 are described, as well as pharmaceutical compositions and therapeutic methods useful for the treatment of cancer.

The present invention relates to the field of biopharmaceutical technology, and particularly, to a method for treating a tumor with a combination of a recombinant oncolytic virus and a macromolecular antibody-based anti-cancer drug. The method comprises: using the recombinant oncolytic virus and the macromolecular antibody-based anti-cancer drug in combination to treat the tumor, wherein the macromolecular antibody anti-cancer drug includes, but is not limited to, macromolecular antibody-based anti-cancer drugs targeting HER2, EGFR, 5T4, B7-H3, TROP2, BCMA, VEGFR-2, SLAMF7, CD3, CD19, CD20, CD22, CD30, CD33, CD38, CD52, CD79b, GD2, VEGF, CTLA4, Claudin18.2, PD-1, PD-L1 and the like, i.e., monoclonal antibody-based drugs, polyclonal antibody-based drugs, antibody-drug conjugates and the like. The method can achieve a therapeutic effect comparable or superior to those of the monotherapies, or even a synergistic effect.

Provided herein are CD70-binding proteins comprising a CD70-binding domain and a transmembrane domain, engineered immune cells comprising the CD70-binding proteins, and methods of making and using the same. Also provided herein are engineered immune cells e.g. CAR (chimeric antigen receptor) T cells for administration to patients to treat cancer (e.g., solid tumors and hematologic tumors) and other unwanted conditions. The cells are engineered to functionally express a first antigen binding molecule e.g. a CD70 CAR and a second antigen binding molecule e.g. a second CAR that binds a target molecule characteristic of the cancer or other disease or unwanted condition. The cells may be further engineered to reduce the functional expression level of one or more of TRAC, CD52 and CD70. Also provided are methods of making and using the engineered cells, compositions and kits comprising them, and methods of treating by administering them.

Provided herein are CD70-binding proteins comprising a CD70-binding domain and a transmembrane domain, engineered immune cells comprising the CD70-binding proteins, and methods of making and using the same. Also provided herein are engineered immune cells e.g. CAR (chimeric antigen receptor) T cells for administration to patients to treat cancer (e.g., solid tumors and hematologic tumors) and other unwanted conditions. The cells are engineered to functionally express a first antigen binding molecule e.g. a CD70 CAR and a second antigen binding molecule e.g. a second CAR that binds a target molecule characteristic of the cancer or other disease or unwanted condition. The cells may be further engineered to reduce the functional expression level of one or more of TRAC, CD52 and CD70. Also provided are methods of making and using the engineered cells, compositions and kits comprising them, and methods of treating by administering them.