Autophagy genes in immunity.

Autophagy genes in immunity.
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DOI:
10.1038/ni.1726
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发表时间:
2009-05
期刊:
影响因子:
30.5
通讯作者:
--
中科院分区:
医学1区
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--
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在经典形式中,自噬是细胞质成分,包括细胞内病原体,被隔离在双膜结合的自噬体中,并被递送到溶酶体降解的途径。这一途径与先天免疫和适应性免疫的各个方面有关,包括病原体耐药性、I型干扰素的产生、抗原呈递、耐受性和淋巴细胞发育,以及细胞因子信号传导和炎症的负调控。这些联系大多来自免疫效应细胞中编码自噬分子的基因失活的研究。然而,目前尚不清楚这些基因在免疫中的所有关键功能是代表“经典自噬”还是这些基因可能的尚未定义的自噬溶酶体独立功能。本文综述了免疫系统中自噬基因失活导致的表型,并讨论了自噬基因在免疫中的多效性功能。
In its classical form, autophagy is a pathway by which cytoplasmic constituents, including intracellular pathogens, are sequestered in a double-membrane–bound autophagosome and delivered to the lysosome for degradation. This pathway has been linked to diverse aspects of innate and adaptive immunity, including pathogen resistance, production of type I interferon, antigen presentation, tolerance and lymphocyte development, as well as the negative regulation of cytokine signaling and inflammation. Most of these links have emerged from studies in which genes encoding molecules involved in autophagy are inactivated in immune effector cells. However, it is not yet known whether all of the critical functions of such genes in immunity represent ‘classical autophagy’ or possible as-yet-undefined autophagolysosome-independent functions of these genes. This review summarizes phenotypes that result from the inactivation of autophagy genes in the immune system and discusses the pleiotropic functions of autophagy genes in immunity.
免疫相关的GTPase IRGM1通过防止干扰素γ诱导的细胞死亡促进活化的CD4+ T细胞群体的扩张。
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