The present study demonstrated that the role of TLR4 in the pathogenesis of SLE disease might be through the suppression of regulatory T cells and the effect of proinflammatory cytokines (such as IL-6 and TNF-α) on SLE pathogenesis, inducing TLR4-mediated neutrophil activation. The gene discussed is TLR4; the disease is systemic lupus erythematosus.