8 results about "CXCR3" patented technology

This invention provides a method for screening peptides that specifically target T cells, comprising providing T cells having a subset selected from CD1, CD2, CD3, CD4, CD5, CD7, CD8, CD16, CD25, CD26, CD27, CD28, CD30, CD38, CD39, CD40L, CD44, CD45, CD62L, CD69, CD73, CD80, CD83, CD86, CD95, CD103, CD119, CD126, CD150, CD152 (CTLA-4), CD153, CD154 (CD40L) The T cells are labeled with at least one of the following surface antigen markers: CD161, CD183, CD223, CD254, CD275, CD45RA, CXCR3, CXCR5, FasL, IL18R1, CTLA-4, OX40, GITR, LAG3, ICOS, PD-1, leu-12, TCR, TLR1, TLR2, TLR3, TLR4, TLR6, NKG2D, CCR, CCR1, CCR2, CCR4, CCR6, and CCR7. The T cells are then contacted with a peptide display library, and target peptides that specifically bind to the T cells are screened therefrom.

Provided is a method for screening polypeptides that specifically target T cells, comprising: providing T cells having a surface antigen marker selected from at least one of CD1, CD2, CD3, CD4, CD5, CD7, CD8, CD16, CD25, CD26, CD27, CD28, CD30, CD38, CD39, CD40L, CD44, CD45, CD62L, CD69, CD73, CD80, CD83, CD86, CD95, CD103, CD119, CD126, CD150, CD152 (CTLA-4), CD153, CD154 (CD40L), CD161, CD183, CD223, CD254, CD275, CD45RA, CXCR3, CXCR5, FasL, IL18R1, CTLA-4, OX40, GITR, LAG3, ICOS, PD-1, leu-12, TCR, TLR1, TLR2, TLR3, TLR4, TLR6, NKG2D, CCR, CCR1, CCR2, CCR4, CCR6, and CCR7; and contacting the T cells with a polypeptide display library, and screening therefrom target polypeptides that specifically bind to the T cells.

Disclosed are nucleic acid constructs encoding CXCR3 and a CAR and cells containing same for the treatment of cancers.

The application belongs to the technical field of biological medicine, and particularly relates to the use of SH2 domain-containing protein tyrosine phosphatase 1 (SHP1) in the preparation of a drug for treating chronic pain, in particular to the use of SHP1 in the preparation of a drug for treating chronic pain by regulating the morphology of spinal cord astrocytes, the integrity of the blood-spinal cord barrier and the STAT1-CXCL10-CXCR3 neuroimmune signal axis, and a chronic pain treatment strategy based on the signal axis. The application first discloses that SHP1 in spinal cord astrocytes directly dephosphorylates STAT1, inhibits the transcription of CXCL10 and the subsequent infiltration of T lymphocytes into the spinal cord, and discloses the core analgesic mechanism, thereby establishing SHP1 as a new target for treating chronic pain, and opening up a new way for the precise treatment of clinical chronic pain, especially neuropathic pain.

The application discloses a research method for the mechanism of CXCR3A in acute respiratory distress syndrome, and relates to the technical field of biomedicine; and comprises the following steps: establishing an animal ARDS model and setting an intervention group; experiment animals are randomly divided into at least four groups, namely a normal control group, an ARDS model group, a CXCR3 broad-spectrum inhibitor intervention group and a CXCR3A selective inhibitor intervention group; a damaging agent is applied to the model group and the two inhibitor intervention groups of animals to establish an ARDS model; the CXCR3 broad-spectrum inhibitor intervention group and the CXCR3A selective inhibitor intervention group are respectively pretreated with corresponding inhibitors before modeling. The method of the application constructs a complete research framework from the whole animal level to the molecular level, covers multiple key aspects of pathological morphology, inflammatory response, oxidative stress and target gene expression, and can reveal the comprehensive mechanism of CXCR3A in the occurrence and development of ARDS.

The invention provides a method for predicting the susceptibility of a patient suffering from a cancer or a myeloid-mediated disease to immunotherapy. Furthermore, the invention provides a method for treating a patient suffering from a cancer or a myeloid-mediated disease with immunotherapy. In accordance with these embodiments, the inventive method includes assaying myeloid cells obtained from the patient prior to treatment for the expression of CXCR3. The invention also provides a genetically engineered myeloid cell (GEMy) in which the expression of CXCR3 is modulated (up- or down-regulated). The invention further provides a composition comprising the inventive GEMy and a pharmaceutically acceptable carrier. The invention also provides a method for treating a patient in need of immunotherapy comprising administering the inventive composition to a patient.

The present application relates to an antigen binding protein targeting CXCR3 and its use, the antigen binding protein can specifically bind CXCR3, comprising a heavy chain variable region and a light chain variable region. The present application also provides a preparation method of the antigen binding protein and its use.

The present application relates to the use of platelet factor 4 in the preparation of a drug for treating or preventing Candida albicans infection, platelet factor 4 acts on macrophage CXCR3 receptor, antagonizes Candida albicans induced macrophage PANoptosis, thereby reducing the damage of Candida albicans to macrophages, maintaining the survival and normal function of macrophages, enhancing the clearance ability of the body to Candida albicans, reducing the inflammatory response caused by infection, reducing pathological damage, and different from the treatment mechanism of traditional antifungal drugs, the present application does not directly act on fungi, which helps to reduce the formation of drug-resistant strains and the toxic side effects such as liver toxicity and kidney toxicity caused by antifungal drugs, and can provide a more optimal new treatment mode for clinical Candida albicans infection.