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自身免疫与脂代谢之间的细胞和分子联系。

Cellular and Molecular Links between Autoimmunity and Lipid Metabolism.

机构信息

Laboratory of Immune Regulation, Institute of Pharmaceutical Sciences, Seoul National University, Seoul 08826, Korea.

These authors contributed equally to this work.

出版信息

Mol Cells. 2019 Nov 30;42(11):747-754. doi: 10.14348/molcells.2019.0196.

Abstract

The incidence of atherosclerosis is higher among patients with several autoimmune diseases such as psoriasis, rheumatoid arthritis (RA) and systemic lupus erythematosus (SLE). It is well documented that innate immune cells including macrophages and dendritic cells sense lipid species such as saturated fatty acids and oxidized low-density lipoprotein and produce pro-inflammatory cytokines and chemokines. However, whether a hyperlipidemic environment also impacts autoimmune T cell responses has been unclear. Among CD4+ T cells, Th17 and follicular helper T (Tfh) cells are known to play pathogenic roles in the development of hyperlipidemiaassociated autoimmune diseases. This review gives an overview of the cellular and molecular mechanisms by which dysregulated lipid metabolism impacts the pathogenesis of autoimmune diseases, with specific emphasis on Th17 and Tfh cells.

摘要

动脉粥样硬化的发病率在患有几种自身免疫性疾病的患者中较高,如银屑病、类风湿关节炎(RA)和系统性红斑狼疮(SLE)。有充分的文献记载表明,先天免疫细胞(包括巨噬细胞和树突状细胞)可以感知脂质种类,如饱和脂肪酸和氧化型低密度脂蛋白,并产生促炎细胞因子和趋化因子。然而,高脂血症环境是否也会影响自身免疫性 T 细胞反应尚不清楚。在 CD4+T 细胞中,Th17 和滤泡辅助 T(Tfh)细胞被认为在高脂血症相关自身免疫性疾病的发展中发挥致病作用。这篇综述概述了失调的脂质代谢影响自身免疫性疾病发病机制的细胞和分子机制,特别强调了 Th17 和 Tfh 细胞。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/db0c/6883973/68a391b37fd1/molce-42-747f1.jpg

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