SLE is a systemic inflammatory disease of connective tissue involving many systems and organs, and can involve the skin, plasma membranes, joints, kidneys, and central nervous system. The etiology and pathogenesis of SLE are not yet clear. Current research suggests that the pathogenesis of SLE has intrinsic factors such as genetics and sex hormones, as well as environmental factors and drugs. The interaction of various factors such as genetic quality, environmental factors, and estrogen levels leads to a decrease in T lymphocytes, a decrease in the function of T suppressor cells, and an overproliferation of B cells, which produce a large number of autoantibodies and combine with the corresponding autoantigens in the body to form the corresponding immune complexes, which are deposited on the skin, joints, small blood vessels, glomeruli, etc., and cause acute and chronic inflammation and tissue necrosis with the participation of complement (e.g. lupus nephritis), or antibodies directly interact with tissue cell antigens, causing cell destruction (e.g., specific antigens of red blood cells, lymphocytes and platelet walls bind with corresponding autoantibodies, causing hemolytic anemia, lymphocytopenia and thrombocytopenia, respectively), thus leading to multisystem damage of the body.