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系统性红斑狼疮(systemic lupus erythematosus,SLE)是一种典型的系统性自身免疫性疾病,其发病机制尚未明确。在SLE患者血清中可检测到多种自身抗体,特别是抗核抗体(antinuclear antibodies,ANA)以及高水平的α干扰素(interferon-alpha,IFN-α)等细胞因子。人类Toll样受体9(Toll-likereceptor9,TLR9)可识别低甲基化(内源性)或非甲基化(外源性)的胞嘧啶-磷酸-鸟嘌呤(cytosine-phosphoric acid-gua-nine,CpG)序列,引起交叉反应,产生多种自身抗体,同时引起细胞因子网络的失衡。虽然TLR9在SLE发病中的确切机制仍未明确,但越来越多的研究表明TLR9在SLE的发生发展中起重要作用。
Systemic lupus erythematosus (SLE) is a typical systemic autoimmune disease whose pathogenesis is not yet clear. A variety of autoantibodies, particularly antinuclear antibodies (ANAs) and high levels of cytokines such as interferon-alpha (IFN-α), are detectable in the serum of SLE patients. Human Toll-like receptor 9 (TLR9) recognizes hypomethylated (endogenous) or unmethylated (exogenous) cytosine-phosphoric acid-gua- nine, CpG) sequences that cause cross-reactions to produce a wide range of autoantibodies while causing an imbalance in the cytokine network. Although the exact mechanism of TLR9 in the pathogenesis of SLE remains unclear, more and more studies indicate that TLR9 plays an important role in the development of SLE.