Systemic lupus erythematosus is a prototypical autoimmune disease characterized by the production of multiple autoantibodies against nuclear components of cells and multisystem involvement. Autoantibodies are of great significance to the diagnosis, treatment, prognosis and clinical research of SLE. The following is a brief analysis of the common autoantibodies in clinical SLE. 1. Immunofluorescence anti-nuclear antibody (IFANA): It is commonly used in the screening examination of lupus and has a sensitivity of 95% and specificity of 65% for the diagnosis of SLE. In addition to SLE, low titer ANA can also be found in other connective tissue diseases, chronic infections, tumors and normal people. 2. Anti-nuclear antibodies (ANAs): ANAs include a series of autoantibodies against antigenic components in the cell nucleus. Among them, anti-double-stranded DNA (ds-DNA) antibodies have a specificity of 95% and a sensitivity of 70%, and its presence suggests disease activity; a subgroup of anti-ds-DNA antibodies has been found to cause nephritis, and its titer correlates with nephritis activity; anti-Sm antibodies have a specificity of 99% and a sensitivity of 25%, and the antibodies are characteristic antibodies of SLE, but have no obvious relationship with disease activity; anti- ribosomal P protein antibody was seen in only a minority of patients but was highly specific for SLE, especially in typical neuropsychiatric lupus, where it was reported to correlate with disease activity, with anti-Sm antibody, anti-DNA antibody and anti-cardiolipin antibody. Anti-nucleosome antibodies also have a high specificity for SLE. Anti-single-stranded DNA, anti-histone, anti-RNP, anti-SSA and anti-SSB antibodies can be found in SLE and other autoimmune diseases with less specificity. Anti-SSA and anti-SSB antibodies are associated with secondary dry syndrome and neonatal lupus. 3. other autoantibodies in SLE include: antiphospholipid antibodies associated with antiphospholipid antibody syndrome (including anti-cardiolipin antibodies and lupus anticoagulant); anti-erythrocyte antibodies associated with hemolytic anemia; anti-platelet antibodies associated with thrombocytopenia; anti-neuronal antibodies associated with psychogenic lupus, etc. SLE patients also often have positive serum rheumatoid factor. Experimental and clinical evidence suggests that some of the autoantibodies mentioned above can play a direct role in the development of disease and are referred to as pathogenic autoantibodies; alternatively, autoantibodies may reflect only disease-specific immune mechanisms and are not themselves pathogenic. Although the pathogenesis of SLE is complex, it is clear that the target tissue damage is mainly caused by pathogenic autoantibodies and immune complexes. The pathogenic autoantibodies in SLE include subsets of antibodies to different antigens including anti-ribosomal P protein antibodies, double-stranded DNA, Ro, NR2, erythrocyte band 3 protein and phospholipids, usually of the IgG type and capable of binding complement, often years before the first clinical signs of the disease. Among the abundant autoantibodies in SLE, pathogenic antibodies are associated with the activity of SLE, and many others have not yet been studied. Happily, immunoadsorption (IA) is now clinically available to remove pathogenic antibodies from the body for the purpose of treating the disease. This is a boon for many patients with SLE combined with severe complications that are difficult to treat.