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I 型干扰素是否在发病机制连续体中连接系统性自身免疫和代谢综合征?

Do Type I Interferons Link Systemic Autoimmunities and Metabolic Syndrome in a Pathogenetic Continuum?

机构信息

Dendritic Cell Biology Laboratory, CSIR-Indian Institute of Chemical Biology (IICB)-Translational Research Unit of Excellence, CN6 Sector V, Salt Lake, Kolkata, West Bengal, 700091, India; Division of Cancer Biology and Inflammatory Disorders, CSIR-Indian Institute of Chemical Biology (IICB), CN6 Sector V, Salt Lake, Kolkata, West Bengal, 700091, India.

出版信息

Trends Immunol. 2018 Jan;39(1):28-43. doi: 10.1016/j.it.2017.07.001. Epub 2017 Aug 17.

Abstract

The central pathogenetic role of type I interferons (IFNs) in several systemic autoimmune diseases is well established. Recent studies have also discovered a similar crucial role of type I IFNs in different components of metabolic disorders. Self nucleic acid-driven Toll-like receptor (TLR) activation in plasmacytoid dendritic cells (pDCs) and type I IFN induction appear to be the key initiating events shared by most of these autoimmune and metabolic diseases. Further strengthening this link, many patients with systemic autoimmunities also present with metabolic disorders. This concurrence of autoimmunities and metabolic disorders may be explained by a single pathogenetic continuum, and suggests shared targets for potential new therapies.

摘要

I 型干扰素(IFNs)在几种系统性自身免疫性疾病中的中心致病作用已得到充分证实。最近的研究还发现,I 型 IFNs 在代谢紊乱的不同成分中也具有类似的关键作用。浆细胞样树突状细胞(pDCs)中自身核酸驱动的 Toll 样受体(TLR)激活和 I 型 IFN 诱导似乎是大多数这些自身免疫和代谢疾病共有的关键起始事件。进一步加强这种联系的是,许多患有系统性自身免疫性疾病的患者也存在代谢紊乱。自身免疫和代谢紊乱的这种并存可以用单一的发病连续统来解释,并提示潜在新疗法的共同靶点。

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