Fueling autoimmunity: type I interferon in autoimmune diseases.

Fueling autoimmunity: type I interferon in autoimmune diseases.
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DOI:
10.1586/eci.12.106
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发表时间:
2013-03
影响因子:
4.4
通讯作者:
Cao W
Cao W
中科院分区:
医学3区
文献类型:
--
作者:
Di Domizio J;Cao W

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近年来,利用基因组、细胞和动物模型方法进行的积极研究揭示了驱动自身免疫性疾病发展的根本力量。I型IFN (IFN)在一系列自身免疫性疾病中具有独特的分子特征。IFN由多种含核酸复合物诱导,可触发浆细胞样树突状细胞(pDCs)的先天免疫激活。IFN启动、激活或分化各种白细胞群以促进自身免疫。因此,在几个实验模型中,IFN信号对于狼疮的发生和/或进展是必不可少的。然而,SLE的异质性需要更好地表征IFN通路如何被激活并随后促进自身免疫性疾病的进展。鉴于I型IFN的核心作用,人们设计了各种策略来针对这些细胞因子或相关途径来抑制自身免疫性疾病的进展。
In recent years, active research using genomic, cellular and animal modeling approaches has revealed the fundamental forces driving the development of autoimmune diseases. Type I IFN (IFN) imprints unique molecular signatures in a list of autoimmune diseases. IFN is induced by diverse nucleic acid-containing complexes, which trigger innate immune activation of plasmacytoid dendritic cells (pDCs). IFN primes, activates or differentiates various leukocyte populations to promote autoimmunity. Accordingly, IFN signaling is essential for the initiation and/or progression of lupus in several experimental models. However, the heterogeneous nature of SLE requires better characterization on how IFN pathways are activated and subsequently promote the advancement of autoimmune diseases. Given the central role of type I IFN, various strategies are devised to target these cytokines or related pathways to curtail the progression of autoimmune diseases.
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