The pathogenesis of SLE remains unclear, and existing studies suggest that genetics, estrogen, pathogenic microbial infections, ultraviolet light, and medications are associated with the development of lupus, and that abnormal immune inflammation is its causative feature. Currently, people with SLE susceptibility genes or family history are considered to be at high risk for lupus development. These people, especially women of childbearing age, are under the influence of estrogen, or infected with certain pathogenic microorganisms, or over-exposed to ultraviolet radiation, or exposed to certain drugs or chemicals, resulting in a disruption of the body’s immune balance, excessive activation of B cells, and the production of a large number of different types of autoantibodies. These autoantibodies do not recognize the body’s own tissue components and treat them as foreign “foreign bodies”, activating antigenic antibody reactions, inducing immune inflammation, causing multi-system organ damage, and leading to morbidity. For patients who have been clearly diagnosed with SLE, factors such as cold, fatigue, mental stress and emotional abnormalities can trigger the disease activity or aggravate the degree of the disease. It can be seen that the pathogenesis of SLE is complex, involving multiple factors such as genetics, estrogen, and environment. No definite cause has been studied.