摘要
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 kind of typical systemic autoimmune disease, and its exact pathogenesis remains unclear. In the serum of SLE patients, we have found varieties of autoantibodies, especially antinuclear antibodies （ANA） , and cytokines including high level of interferon-alpha （IFN-α）. The human Toll-like receptor 9 （ TLR9 ） can identify low methylation （endogenous） or unmethylated （exogenous） cytosinephosphoric acid-guanine（CpG） motif, leading to cross reaction, producing a broad variety of autoantibodies and causing the unbalance of cytokine network. Although the behaviour of TLR9 in the precise pathogenesis of SLE remains largely unknown, more and more studies suggest that TLR9 plays a critical role in the development of SLE.
出处
《中国皮肤性病学杂志》
CAS
北大核心
2012年第10期945-947,共3页
The Chinese Journal of Dermatovenereology
基金
国家自然科学基金资助(81060251)
