Introduction
Systemic lupus erythematosus (SLE) is an autoimmune disease characterized the production of antibodies against components of the cell nucleus resulting in extensive clinical manifestations. LES primarily affects young women with a peak incidence at 15-40 years of age during the reproductive years with the ratio of women and men 5:1. Unclear etiology were related to the specific immune response in major histocompatibility complex class II, HLA-DR2 and HLA-DR3.Pathogenesis of SLE
The existence of genetic factors play an important role in disease susceptibility serrta expression. Especially the role that genes encoding elements of the immune system. Among certain MHC HLA-DR2 and especially HLA-DR3 and the complement components that play a role in the early phase of complement binding reaction, namely; C1q, C1r,, C1s, C4 and C2).The existence of one or several factors right trigger in individuals who have a genetic predisposition to produce abnormal driving force for CD4 + T cells. Resulting in the loss of tolerance of autoreactive T cells that would lead to the induction and expansion of B cells, both of which produce autoantibodies or a memory cell. These antibodies are jointly called ANA (antinuclear antibody). Specific to the antigen, ANA forming immune complexes circulating in the circulation.

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