Links between autophagy, innate immunity, inflammation and Crohn's disease.

Links between autophagy, innate immunity, inflammation and Crohn's disease.
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DOI:
10.1159/000228557
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发表时间:
2009
期刊:
Digestive diseases (Basel, Switzerland)
影响因子:
--
通讯作者:
Deretic V
Deretic V
中科院分区:
其他
文献类型:
--
作者:
Deretic V

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自噬是一种基本的生物学过程,它赋予真核细胞自消化自身细胞质的能力。自噬在衰老、发育、神经变性、癌症和免疫中起作用。自噬的免疫学作用首先被认为是自噬通过杀死细胞内微生物来净化细胞内部的能力,并且间接地通过成功的细胞内病原体进化以保护自己免受自噬的适应。从那时起,免疫中自噬功能的库已经被极大地扩展到包括调节和效应器性质与先天性和适应性免疫的许多交叉点。自噬作为模式识别受体的效应器和调节器,它支持MHC II呈递细胞质中的(自身和微生物)抗原,它通过T细胞库的胸腺选择形成中枢耐受,是Th 1/Th 2极化的效应物,影响T、B和特化免疫细胞如潘氏细胞的稳态,并且,当有缺陷时,可能是人类群体中慢性炎性病症如克罗恩病的促成因素。
Autophagy is a fundamental biological process that endows eukaryotic cells with the ability to autodigest portions of their own cytoplasm. Autophagy plays roles in aging, development, neurodegeneration, cancer, and immunity. The immunological role of autophagy was first recognized for the ability of autophagy to sanitize the cellular interior by killing intracellular microbes, and indirectly by the adaptations that successful intracellular pathogens have evolved to protect themselves from autophagy. Since then, the repertoire of autophagy functions in immunity has been vastly expanded to include numerous intersections of regulatory and effector nature with innate and adaptive immunity. Autophagy acts both as an effector and a regulator of pattern recognition receptors, it supports MHC II presentation of cytosolic (self and microbial) antigens, it shapes central tolerance via thymic selection of T cell repertoire, is an effector of Th1/Th2 polarization, affects homeostasis of T, B, and specialized immune cells such as Paneth cells, and, when defective, can be a contributing factor to chronic inflammatory conditions in human populations such as Crohn’fs disease.
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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