Endosomal Toll-like receptors in autoimmunity: mechanisms for clinical diversity.
Endosomal Toll-like receptors in autoimmunity: mechanisms for clinical diversity.
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DOI：
10.2217/thy.09.2
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发表时间：
2009-05-01
期刊：
影响因子：
--
通讯作者：
Greidinger EL
中科院分区：
文献类型：
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作者：
Trivedi S;Greidinger EL
核内体Toll样受体（TLR3、TLR7和TLR9）参与自身免疫性疾病的发病机制。它们的信号通路显示出显著的相似性，然而这些TLR中的每一个激活后的结果导致临床上不同的自身免疫性疾病表型。这篇评论讨论了如何可能出现的差异，在分子和细胞水平，以解释这种多样性的反应。了解单个TLR途径的作用以及它们与非TLR先天免疫途径在疾病（如系统性狼疮性肾炎）发病机制中的关系，突出了这种自身免疫性疾病谱的潜在治疗靶点。
The endosomal Toll-like receptors (TLR3, TLR7 and TLR9) have been implicated in the pathogenesis of autoimmune diseases. Their signaling pathways show remarkable similarities and yet the outcomes following activation of each of these TLRs lead to clinically distinct autoimmune disease phenotypes. This review discusses how differences may arise at a molecular and cellular level to account for this diversity of responses. Understanding the roles of individual TLR pathways and the relationships between them and non-TLR innate immune pathways in the pathogenesis of diseases such as systemic lupus erythematosis highlights potential treatment targets for this spectrum of autoimmune diseases.