Pathogenic autoantibodies in SLE patients bind to antigens and form immune complexes (ICs) deposited in target organs, which can activate TLR on DCs and produce large amounts of type I IFNs, especially IFN-α and IFN receptors to promote a series of autoimmune responses in CD4+ T lymphocytes, CD8+ T lymphocytes and B cells, causing abnormal immune regulation. The gene discussed is CD4; the disease is systemic lupus erythematosus.