Autophagy and autoimmunity crosstalks.
Autophagy and autoimmunity crosstalks.
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自噬和自身免疫串扰。
DOI：
10.3389/fimmu.2013.00088
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发表时间：
2013
影响因子：
7.3
通讯作者：
Eissa NT
中科院分区：
文献类型：
--
作者：
Bhattacharya A;Eissa NT
自噬，最初被认为是一种保守的大量降解机制，已成为众多免疫功能的核心参与者。自噬在宿主防御细胞内和细胞外病原体、代谢综合征、免疫细胞稳态、抗原加工和呈递以及维持耐受性中是重要的。上述过程与触发或加剧自身免疫有关的观察结果提出了自噬参与介导自身免疫过程的可能性，无论是直接还是作为该途径介导的先天或适应性功能的结果。全基因组关联研究表明，自噬相关基因5（Atg5）和Atg16l1的单核苷酸多态性（SNP）分别与系统性红斑狼疮（SLE）和克罗恩病的易感性相关。Atg5的表达增强也报道了在血液中的小鼠实验性自身免疫性脑脊髓炎（EAE），多发性硬化症（MS）的小鼠模型，并在T细胞分离的血液或脑组织中的活跃复发的MS患者。本文综述探讨了自噬途径在先天性和适应性免疫系统中的作用，调节或介导的发病，进展，或自身免疫过程的恶化。
Autophagy, initially viewed as a conserved bulk-degradation mechanism, has emerged as a central player in a multitude of immune functions. Autophagy is important in host defense against intracellular and extracellular pathogens, metabolic syndromes, immune cell homeostasis, antigen processing and presentation, and maintenance of tolerance. The observation that the above processes are implicated in triggering or exacerbating autoimmunity raises the possibility that autophagy is involved in mediating autoimmune processes, either directly or as a consequence of innate or adaptive functions mediated by the pathway. Genome-wide association studies have shown association between single nucleotide polymorphisms (SNPs) in autophagy related gene 5 (Atg5), and Atg16l1 with susceptibility to systemic lupus erythematosus (SLE) and Crohn’s disease, respectively. Enhanced expression of Atg5 was also reported in blood of mice with experimental autoimmune encephalomyelitis (EAE), a mouse model of multiple sclerosis (MS), and in T cells isolated from blood or brain tissues from patients with active relapse of MS. This review explores the roles of autophagy pathway in the innate and adaptive immune systems on regulating or mediating the onset, progression, or exacerbation of autoimmune processes.
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影响因子：
5.2
作者：
Goldbach-Mansky R
通讯作者：
Goldbach-Mansky R
影响因子：
30.5
作者：
通讯作者：
--
DOI：
10.1073/pnas.0902745106
发表时间：
2009-04-28
影响因子：
11.1
作者：
Ben-Sasson, Shlomo Z.;Hu-Li, Jane;Paul, William E.
通讯作者：
Paul, William E.
影响因子：
7.5
作者：
Giuliani, Fabrizio;Grieve, Adam;Rabouille, Catherine
通讯作者：
Rabouille, Catherine
影响因子：
15.9
作者：
Espert, Lucile;Denizot, Melanie;Biard-Piechaczyk, Martine
通讯作者：
Biard-Piechaczyk, Martine