25 results about "CD74" patented technology

The invention relates to an in vitro or ex vivo method for determining the risk of death for a subject infected with a respiratory virus, said method comprising the steps of measuring, in a biological sample from said subject, the expression level of the OAS2 gene, and comparing the expression level thus measured or a value derived from this amount to a predetermined reference value. The method thus makes it possible to conclude that there is an increased risk of death for the subject when a sub-expression of the OAS2 gene is statistically demonstrated from the biological sample. Advantageously, the measurement of the expression level of OAS2 can be supplemented by a measurement of one or more additional genes such as C3ARI, CD177, ADGRE3, CIITA, IL-10, ILIR2, CD74, TDRD9 and combinations thereof. Kits for measuring the expression of OAS2 and optionally one or more additional genes are also disclosed.

The invention discloses a method for detecting non-target cells in amniotic epithelial cells, which comprises reagents for detecting one or more of the following gene markers: FCGBP, RNASE6, DAB2, STAB1, RAB3IL1, CSF1R, CD68, CD209, EGFL7, LGALS2, LILRB4, HLA-DMB, HLADMA, CD74, ANPEP, CD44, CCR7, CD3G, CD3D, CD27, CD5, SPOCK2, TCF7, GZMH, KLRC2 and the like. Wherein the non-target cells are selected from macrophage-like cells, monocyte-like cells, T cell-like cells, NK cell-like cells, myeloid-like cells and neutrophil-like cells, a detection method is provided for quality control of the amniotic epithelial cells, and guidance is also provided for a cell product preparation process.

The present invention relates to an inhibitor of CD74 protein activity or expression, for the therapeutic use thereof in the prevention and / or treatment of chronic inflammatory diseases including: chronic inflammatory rheumatisms, chronic inflammatory dermatoses, chronic inflammatory bowel diseases and chronic inflammatory neurological diseases. In another embodiment, the invention relates to an isolated anti-CD74 antibody or fragment thereof, comprising six CDRs having the sequences SEQ ID NO. 3, 4, 5, 11, 12, and 13.

The invention belongs to the technical field of medicines, and discloses a KRT6A gene expression inhibitor and application thereof in preparation of a medicine for treating gemcitabine drug-resistant pancreatic cancer. Researches find that KRT6A is abnormally highly expressed in pancreatic cancer and is closely related to poor curative effect of gemcitabine. According to the inhibitor, KRT6A gene expression is specifically silenced in a tumor targeted delivery mode, expression and functions of nucleoside transporter ENT1 are recovered, and cellular uptake of gemcitabine is enhanced; the compound can inhibit MIF-CD44 / CD74 signal axis mediated tumor-associated macrophage M2 type polarization, reduce exogenous pyrimidine nucleoside supply and weaken competitive inhibition of the compound and gemcitabine in nucleoside transport and metabolic pathways, so that effective uptake and efficacy of gemcitabine in pancreatic cancer cells are synergistically improved, and gemcitabine drug resistance is reversed or relieved. The invention provides a new and effective technical scheme for clinical treatment of gemcitabine drug-resistant pancreatic cancer.

The invention relates to the technical field of medicines, in particular to application of a CD74 gene as a molecular marker in preparation of a bladder cancer immunotherapy curative effect prediction reagent. A mouse bladder cancer subcutaneous tumor model shows that the CD74 inhibits the occurrence and development of the bladder cancer, a bladder cancer patient with high expression of the CD74 has better response to immunotherapy, and it is indicated that the CD74 inhibits the occurrence and development of the bladder cancer and serves as a bladder cancer immunotherapy marker.

The invention relates to the technical field of cellular immunotherapy, and discloses an application of a CD74 positive regulatory T cell in treatment of graft versus host disease, the CD74 positive regulatory T cell is composed of the following components in proportion: in a sorted and purified cell population, the proportion of regulatory T cells with CD4 + CD25 + CD127-phenotype is 85-95%, the proportion of regulatory T cells with CD25 + CD127-phenotype is 1-5%, and the proportion of regulatory T cells with CD24 + CD25 + CD127-phenotype is 1-5%. Wherein the CD74 high-expression subgroup accounts for 60-75% of the total amount of the regulatory T cell, the cell subgroup functional immune molecule combination comprises CTLA4, FOXP3, TIGIT and TNFRSF18, when the CD74 positive regulatory T cell is used for treating graft versus host disease, the CD74 positive regulatory T cell is firstly used for preventive infusion, single infusion is performed on the day of transplantation, the dosage is 5 * 10 < 5 > cells / receptor, and then the CD74 positive regulatory T cell is used for treating the graft versus host disease. The CD74 positive regulatory T cells are used for repeated therapeutic infusion when early aGVHD symptoms occur, graded treatment is carried out, pathological immune response is inhibited to the maximum extent, immune tolerance is promoted, the treatment is carried out once a week and 2-3 times in total, and the dosage of each time is 1 * 10 < 6 > cells / receptor.

The antibodies of the present invention have specific binding activity to HLA-DQ2.5 and may have binding activity to HLA-DQ2.2 and / or HLA-DQ7.5, but substantially no binding activity to HLA-DQ8, HLA-DQ5.1, HLA-DQ6.3, HLA-DQ7.3, HLA-DR, HLA-DP, or a complex of the invariant chain (CD74) and HLA-DQ2.5. The antibodies bind to HLA-DQ2.5 in the presence of a gluten peptide such as gliadin, i.e., bind to HLA-DQ2.5 forming a complex with the gluten peptide. The antibodies have neutralizing activity against the binding between HLA-DQ2.5 and TCR, and thus block the interaction between HLA-DQ2.5 and an HLA-DQ2.5-restricted CD4+ T cell. The antibodies do not undergo rapid internalization mediated by the invariant chain.

The invention relates to an in vitro or ex vivo determination method for determining the risk of death of a patient infected by a respiratory virus, said method comprising the steps of measuring, in a biological sample from said patient, the expression level of the ADGRE3 gene, and of comparing the expression level thus measured or a value derived from this quantity with a predetermined reference value. The method thus makes it possible to conclude that there is an increased risk of death of the patient when an underexpression of the ADGRE3 gene is statistically demonstrated from the biological sample. Advantageously, the measurement of the expression level of ADGRE3 can be supplemented by the measurement of one or more additional genes such as C3AR1, CD177, OAS2, CIITA, IL-10, IL1R2, CD74, TDRD9) and combinations thereof. The invention also relates to kits for measuring the expression of ADGRE3 and optionally of one or more additional genes.

The present invention relates to an inhibitor of CD74 protein activity or expression, for therapeutic use in the prevention and / or treatment of a chronic inflammatory disease selected from: chronic inflammatory rheumatic diseases, chronic inflammatory dermatoses, chronic inflammatory bowel diseases, and chronic inflammatory neurological diseases. In another aspect, the invention relates to an isolated anti-CD74 antibody or fragment thereof, comprising at least one CD74 receptor (CDR) having a sequence selected from SEQ ID NO. 1 to 5.

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.

The invention belongs to the field of biology, and provides an anti-CD74 antibody or an antigen binding fragment and application thereof, the antibody or the antigen binding fragment comprises VH CDR1, VH CDR2 and VH CDR3 as shown in SEQ ID NO: 2, SEQ ID NO: 3 and SEQ ID NO: 4, and VL CDR1, VL CDR2 and VL CDR3 as shown in SEQ ID NO: 6, SEQ ID NO: 7 and SEQ ID NO: 8. The anti-CD74 antibody disclosed by the invention has remarkable specific binding property with CD74, is high in binding affinity and has a good patent medicine prospect.

The invention relates to an in vitro or ex vivo method for determining the risk of death in a subject infected with a respiratory virus, for example SARS-CoV-2, comprising a measurement, in a biological sample of said subject, of the level of expression of the CD74 gene; the invention also relates to associated kits.

Provided are an anti-CD74 antibody or an antigen-binding fragment thereof, a preparation method therefor and the use thereof, and an antibody-drug conjugate, and a preparation method therefor and the use thereof. The anti-CD74 antibody can specifically bind to CD74. The antibody-drug conjugate has application prospects in the treatment of immune diseases.

The present invention relates to granulocyte precursor cell that has been differentiated in vitro, wherein the granulocyte precursor cell comprises: (a) increased expression of one or more of: serglycin (SRGN), myeloperoxidase (MPO), major histocompatibility complex, class II, DR alpha (HLA-DRA), CD74, and elastase (ELANE) when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo; and / or (b) decreased expression of one or more of: defensin alpha 1 (DEFA1), defensin alpha 3 (DEFA3), cathelicidin antimicrobial peptide (CAMP), bactericidal permeability increasing protein (BPI), and azurocidin 1 (AZU1) when compared to an equivalent granulocyte precursor cell that has been differentiated in vivo. Also provided are cells, methods for producing the same, uses of the same, and kits comprising the same.

The antibodies of the present invention have specific binding activity to HLA-DQ2.5 and may have binding activity to HLA-DQ2.2 and / or HLA-DQ7.5, but substantially no binding activity to HLA-DQ8, HLA-DQ5.1, HLA-DQ6.3, HLA-DQ7.3, HLA-DR, HLA-DP, or a complex of the invariant chain (CD74) and HLA-DQ2.5. The antibodies bind to HLA-DQ2.5 in the presence of a gluten peptide such as gliadin, i.e., bind to HLA-DQ2.5 forming a complex with the gluten peptide. The antibodies have neutralizing activity against the binding between HLA-DQ2.5 and TCR, and thus block the interaction between HLA-DQ2.5 and an HLA-DQ2.5-restricted CD4+ T cell. The antibodies do not undergo rapid internalization mediated by the invariant chain.

This invention belongs to the field of biomedical technology, specifically relating to the application of a substance targeting the MIF-CD74 axis in the preparation of drugs for treating male breast cancer. Based on single-cell sequencing data analysis and experimental verification, this invention reveals for the first time the existence of a specific "epithelial cell MIF-macrophage CD74" signaling axis in male breast cancer. This mechanism promotes tumor immune escape by mediating the immunosuppressive M2 polarization of TREM2+ macrophages. This invention proposes to block this axis using anti-MIF antibodies, anti-CD74 antibodies, or small molecule inhibitors to inhibit macrophage M2 polarization and restore anti-tumor immune responses. Furthermore, it provides pharmaceutical compositions containing the above substances, combination therapy regimens, and the application of MIF, CD74, and TREM2 as biomarkers for the diagnosis or prognosis of male breast cancer. This invention provides a novel strategy with high specificity and a clearly defined mechanism for the treatment of male breast cancer.

The invention relates to the technical field of neuroscience and drugs, and discloses application of parecoxib as an MEF2A transcription inhibitor in preparation of antiepileptic drugs, which is characterized in that the parecoxib is in targeted combination with N-terminal alpha1 helix and MADS box structural domain of MEF2A protein to inhibit DNA binding capacity of MEF2A, so that downstream NEK7 / CD74 gene transcription is blocked, and microglial cell mediated neuroinflammation is reduced; according to the present invention, the transcriptional activity action mechanism of parecoxib is inhibited through the MEF2A targeting DNA binding interface, specifically, the parecoxib is specifically bound with the N-terminal alpha 1 helix (residues ARG17, THR20, PHE21, LYS23 and ARG24) and MADS box structure domain of MEF2A so as to inhibit the conformational change and the DNA binding ability (the molecular docking simulation shows the high affinity binding), and the transcription of the downstream target gene (such as NEK7 and CD74) is inhibited by blocking the binding of the MEF2A and the DNA so as to inhibit the transcriptional activity of the MEF2A; therefore, the activation of NLRP3 inflammasomes is reduced; excessive activation of microglial cells is inhibited, and the steady state of the neural network is maintained.

The invention discloses a CD74 gene expression-deleted recombinant cell and a construction method and application thereof, and belongs to the technical field of gene engineering. The CD74 inactivated recombinant cell is obtained in the eukaryotic cell through a gene knockout means, the titer of the corresponding virus can be improved after the recombinant cell is infected with the virus, and the virus with the titer capable of being remarkably improved can be VSV, NDV or other RNA viruses. The invention provides an efficient amplification method for the fields of vaccine development based on the RNA virus, antiviral drug screening and the like, so that a basis is provided for producing, researching and developing anti-RNA virus vaccines or candidate drugs.

The invention discloses a pMHC binding agent and application thereof. The antigen peptide-major histocompatibility complex binding agent comprises four RNA molecules, wherein the first RNA molecule comprises an antigen peptide, a DRB1 * 13: 02 beta chain, a mouse I-Eb binding segment and nucleic acid molecules coded by CD28 and CD3 zeta proteins of transmembrane and intracellular segments; the second RNA molecule comprises CMV, CD74, an antigen peptide and a nucleic acid molecule coded by a red visible spectrum fluorescent protein; the third RNA molecule comprises CD4 and a nucleic acid molecule coded by a T cell surface receptor binding region peptide sequence; and the fourth RNA molecule comprises mCD40L and a nucleic acid molecule coded by a binding peptide fragment for recognizing pMHC. According to the present invention, the antigen peptide-major histocompatibility complex II type molecule and the T cell surface receptor can be efficiently and specifically combined so as to promote the activation of the target cell surface receptor so as to achieve the efficient autoimmune reaction;

The present invention relates to a method for determining a transcriptome score (TScore) suitable for assessing the risk of an undesirable clinical outcome of a patient in a clinical environment from an assay sample or population of assay samples previously extracted from the patient, the method comprising, among other steps, determining a transcriptome score (TScore) suitable for assessing the risk of an undesirable clinical outcome of the patient, gene expression values of at least two different genes selected from a predetermined set of genes are measured for a patient sample or a population of samples previously obtained from the patient, and a transcriptome score is determined, where the genes are assigned or not assigned scores. The method may be computer implemented. The genes of the predetermined set of genes may be at least two genes selected from the group consisting of ADGRE3, ARL14EP, BPGM, C3AR1, CCNB1IP1, CD177, CD274, CD3D, CD74, CIITA, CTLA4, CX3CR1, GNLY, IFNgamma, IL10, IL1R2, IL1RN, IL7R, IP10 / CXCL10, MDC1, OAS2, S100A9, TAP2, TDRD9, TNF, and ZAP70. The method may be performed on an assay biological sample extracted from a patient who has been treated in a resuscitation department, an intensive care unit, or a continued care unit. The invention also relates to a method of classifying samples previously taken from a patient as a group reflecting the risk of an undesirable clinical outcome in a clinical environment, or a method of identifying a patient at risk of an undesirable clinical outcome in a clinical environment, and an in vitro or ex vivo method of screening for whether a drug has the ability to alleviate an undesirable clinical outcome in a patient. The invention also relates to a computer device for carrying out the invention, and to the use of a kit for carrying out the method of the invention.

The present invention relates to therapeutic immunoconjugates comprising SN-38 attached to an antibody or an antigen-binding antibody fragment. The antibody can bind to EGP-1 (TROP-2), CEACAM5, CEACAM6, CD74, CD19, CD20, CD22, CSAp, HLA-DR, AFP or MUCSac, and the immunoconjugate can be administered in a dose of between 4 mg / kg and 24 mg / kg, preferably in a dose of 4, 6, 8, 9, 10, 12, 16 or 18 mg / kg. When administered at specified doses and regimens, the immunoconjugates can reduce the size of solid tumors, reduce or eliminate metastasis, and are effective in treating cancers that are resistant to standard therapies such as radiation therapy, chemotherapy, or immunotherapy.

The present disclosure provides a chimeric antigen receptor (CAR) polypeptide comprising a CD74 antigen binding domain, a transmembrane domain, an intracellular signaling domain, and a co-stimulatory signaling region. Also provided herein is an isolated nucleic acid encoding a recombinant polypeptide as disclosed herein, a vector comprising the isolated nucleic acid, and a cell comprising the vector. Also provided herein is a method of treating lymphoma in a subject in need thereof, the method comprising administering to the subject a therapeutically effective amount of a chimeric antigen receptor polypeptide as disclosed herein. Also described herein is a method of reducing tumor activity in a subject having lymphoma comprising administering to the subject a therapeutically effective amount of a chimeric antigen receptor polypeptide as described herein.

The present invention relates to therapeutic immunoconjugates comprising SN-38 attached to an antibody or antigen-binding antibody fragment. The antibody may bind to EGP-1 (TROP-2), CEACAM5, CEACAM6, CD74, CD19, CD20, CD22, CSAp, HLA-DR, AFP or MUC5ac and the immunoconjugate may be administered at a dosage of between 4 mg / kg and 24 mg / kg, preferably 4, 6, 8, 9, 10, 12, 16 or 18 mg / kg. When administered at specified dosages and schedules, the immunoconjugate can reduce solid tumors in size, reduce or eliminate metastases and is effective to treat cancers resistant to standard therapies, such as radiation therapy, chemotherapy or immunotherapy.

The invention discloses application of D74 as a biomarker in preparation of a kit for evaluating or diagnosing bullous pemphigus. The CD74 expression of the skin lesion part of a to-be-detected subject and the CD74 expression of the corresponding position of the normal skin are compared, bullous pemphigus is positive if the CD74 at the skin lesion part is linearly deposited along the true epidermis junction, and the normal tissue is not positively stained. A BP characteristic gene module is identified by adopting a multi-omics integration analysis strategy, and it is found that the CD74 expression level is remarkably related to the eosinophilic granulocyte infiltration degree; the potential of the aptamer as a diagnostic biomarker is verified in patient tissues through immunohistochemistry, the detection sensitivity is 100%, the specificity is 83.3%, the positive predictive value is 78.9%, and the accuracy is 89.7%.

The invention belongs to the technical field of biological medicine, particularly relates to application of receptor protein CD74 as a vitiligo molecular marker and a treatment target, provides application of the receptor protein CD74 as a vitiligo related molecular marker in diagnosis and treatment for the first time, and determines the effective effect of the receptor protein CD74 in the aspect of vitiligo diagnosis. The blank that no specific laboratory diagnostic index for leucoderma exists at present is filled, and meanwhile, a new target spot is provided for treatment of leucoderma.