Previous studies have indicated that the interplay of antigen-presenting cells (APCs), auto-activated CD4+T cells and B cells can promote autoantibody and inflammatory cytokine production, which plays an important role in the pathogenesis of SLE (4–6).Several studies have shown that CD4+T helper (Th) cell subsets, including Th1, Th2, Th17 and Th22 cells, play critical roles in the immunopathogenesis of SLE (6–8). This evidence concerns the gene CD4 and systemic lupus erythematosus.