Background and ObjectiveSystemic lupus erythematosus (SLE) is an inflammatory autoimmune disorder that may affect multiple organ systems. Lupus nephritis(LN) is a frequent serious complication of SLE which incidence is 2/3 to 3/4. Female greatly outnumber males by 12.5:1. Renal biopsy is a regular examination in SLE to diagnosis 80-100% renal damage. LN is the most common secondary glomerulonephritis. SLE is characterized by abnormality of immune regulation which contribute to the activation and clonal expansion of T-lymphocyte B cells, leading antibodies excess production and immune complexes formation. Helper T lymphocyte and cytokine play important role in the pathogenesis of autoimmune diseases. The imbalance of Thl and Th2 cell is the key cause in the development of serious SLE. LN is the main mortality and morbidity of SLE. Although the pathogenesis of LN is complex, it is well accepted that LN is a kind of immune complex induced disease. Mohan et al showed that there were four mechanism involved in the development of LN: 1. B cell produced antibody against DNA; 2. Helper T cells were involved in the activation of B cell; 3. anti-DNA antibody and immune complex induced renal damage ; 4. increase of nucleosome and the emerge of abnormal nucleosome.
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