Research progress of programmed cell death-1 and its ligand in autoimmune diseases

Autoimmune disease is a disease wherein the body reacts to its own antigen and then attacks and damages tissues. This phenomenon is mainly caused by the activation of T cells. However, other immune cells such as B cells and dendritic cells also participate in the process of the disease. As a negative costimulatory molecule, programmed cell death-1(PD-1) is a 50-55 kDa transmembrane protein encoded by programmed cell death-1, gene on chromosome 2. It is a new member of the immunoglobulin gene superfamily isolated from apoptotic cells by subtractive method. It belongs to the immunoglobulin superfamily with inducible costimulator, CD28 and cytotoxic T-lymphocyte-associated protein 4. PD-1 has two ligands: programmed cell death-ligand 1(PD-L1) and PD-L2. By combining with their ligands, PD-1 can inhibit the activation of T cells and the production of cytokines, which plays an extremely important role in maintaining peripheral immune tolerance. PD-1 has two expression forms: membrane binding protein and soluble protein. Amongst them, membrane PD-1 plays a negative immunoregulation role by directly binding with ligands, whereas soluble PD-1 has the function of binding with PD-Ls, blocking the binding between membrane PD-1 and PD-Ls and interfering with PD-1/PD-Ls-mediated T cell proliferation inhibition. In recent years, PD-1 antibody has shown excellent efficacy in the targeted treatment of malignant tumours. Rheumatic complications such as arthritis, myalgia, secondary Sjogren's syndrome and vasculitis have also been observed in patients with autoimmune disease. With the establishment of PD-1 gene deficient mouse model, more and more research institutions are paying attention to the role of the PD-1 signalling pathway in autoimmune diseases. This paper summarises the research progress of PD-1 and its ligand in autoimmune diseases.