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Current understanding of CTLA-4: from mechanism to autoimmune diseases

Md. Munnaf HossenDepartment of Immunology, Biological Therapy Institute, Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Health Science Center, Shenzhen University, Shenzhen, ChinaYanmei MaDepartment of Immunology, Biological Therapy Institute, Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Health Science Center, Shenzhen University, Shenzhen, ChinaZhihua YinJoint Research Laboratory for Rheumatology of Shenzhen University Health Science Center and Shenzhen Futian Hospital for Rheumatic Diseases, Shenzhen, ChinaYuhao XiaDepartment of Immunology, Biological Therapy Institute, Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Health Science Center, Shenzhen University, Shenzhen, ChinaJing DuDepartment of Laboratory Medicine, Peking University Shenzhen Hospital, Shenzhen, ChinaJim Yi HuangDepartment of Chemistry and Biochemistry, University of Oklahoma, Norman, OK, United StatesJennifer Jin HuangDepartment of Chemistry and Biochemistry, University of Oklahoma, Norman, OK, United StatesLinghua ZouZhizhong YeJoint Research Laboratory for Rheumatology of Shenzhen University Health Science Center and Shenzhen Futian Hospital for Rheumatic Diseases, Shenzhen, ChinaZhong HuangDepartment of Immunology, Biological Therapy Institute, Guangdong Provincial Key Laboratory of Regional Immunity and Diseases, Health Science Center, Shenzhen University, Shenzhen, China
2023en
ABI

Annotatsiya

Autoimmune diseases (ADs) are characterized by the production of autoreactive lymphocytes, immune responses to self-antigens, and inflammation in related tissues and organs. Cytotoxic T-lymphocyte antigen 4 (CTLA-4) is majorly expressed in activated T cells and works as a critical regulator in the inflammatory response. In this review, we first describe the structure, expression, and how the signaling pathways of CTLA-4 participate in reducing effector T-cell activity and enhancing the immunomodulatory ability of regulatory T (Treg) cells to reduce immune response, maintain immune homeostasis, and maintain autoimmune silence. We then focused on the correlation between CTLA-4 and different ADs and how this molecule regulates the immune activity of the diseases and inhibits the onset, progression, and pathology of various ADs. Finally, we summarized the current progress of CTLA-4 as a therapeutic target for various ADs.

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