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自身免疫中的Toll样受体,特别涉及系统性红斑狼疮。

Toll-like receptors in autoimmunity with special reference to systemic lupus erythematosus.

作者信息

Pradhan Vandana D, Das Swaptagni, Surve Prathamesh, Ghosh Kanjaksha

机构信息

Department of Autoimmune Disorders, National Institute of Immunohaematology, Indian Council of Medical Research, KEM Hospital, Parel, Mumbai, India.

出版信息

Indian J Hum Genet. 2012 May;18(2):155-60. doi: 10.4103/0971-6866.100750.

Abstract

The Toll-like receptor (TLR) family plays a fundamental role in host innate immunity by mounting a rapid and potent inflammatory response to pathogen infection. TLRs recognize distinct microbial components and activate intracellular signaling pathways that induce expression of host inflammatory genes. Several studies have indicated that TLRs are implicated in many inflammatory and immune disorders. Extensive research in the past decade to understand TLR-mediated mechanisms of innate immunity has enabled pharmaceutical companies to begin to develop novel therapeutics for the purpose of controlling an inflammatory disease. The roles of TLRs in the development of autoimmune diseases have been studied. TLR7 and TLR9 have key roles in production of autoantibodies and/or in development of systemic autoimmune disease. It remains to be determined their role in apoptosis, in the pathogenesis of RNA containing immune complexes, differential expression of TLRs by T regulatory cells.

摘要

Toll样受体(TLR)家族通过对病原体感染发起快速而有效的炎症反应,在宿主天然免疫中发挥着基础性作用。TLR识别不同的微生物成分,并激活诱导宿主炎症基因表达的细胞内信号通路。多项研究表明,TLR与许多炎症和免疫紊乱有关。在过去十年中,为了解TLR介导的天然免疫机制进行了广泛研究,这使得制药公司能够开始开发用于控制炎症性疾病的新型疗法。TLR在自身免疫性疾病发展中的作用已得到研究。TLR7和TLR9在自身抗体产生和/或全身性自身免疫疾病发展中起关键作用。它们在细胞凋亡、含RNA免疫复合物的发病机制以及调节性T细胞对TLR的差异表达中的作用仍有待确定。

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