The main immunological mechanism in the pathogenesis of SLE is immune dysfunction. Most scholars now believe that some foreign and endogenous antigens act on patients with abnormal immune function, causing B lymphocytes to proliferate in a highly active manner, producing a large number of autoantibodies and binding with the corresponding antigens to form immune complexes deposited in the glomerulus, thus damaging the kidney and causing lupus nephritis. Immune complexes can also damage the kidney. Defects in some complement components and reduced density of certain receptors on erythrocytes and phagocytes, which decrease the ability to clear immune complexes, can aggravate the deposition of immune complexes in the tissues, thus increasing tissue damage. The high incidence of lupus nephritis is related to the abundant blood flow in the kidney and the special structure of the kidney tissue itself that easily allows the deposition of antigens, antibodies and immune complexes.