Autophagy in immunity and inflammation

被引：2667

作者：

Levine, Beth ^{[1
,2
,3
]}

Mizushima, Noboru ^{[4
]}

Virgin, Herbert W. ^{[5
,6
]}

机构：

[1] Univ Texas SW Med Ctr Dallas, Dept Internal Med, Dallas, TX 75390 USA

[2] Univ Texas SW Med Ctr Dallas, Dept Microbiol, Dallas, TX 75390 USA

[3] Univ Texas SW Med Ctr Dallas, Howard Hughes Med Inst, Dallas, TX 75390 USA

[4] Tokyo Med & Dent Univ, Dept Physiol & Cell Biol, Bunkyo Ku, Tokyo 1138519, Japan

[5] Washington Univ, Sch Med, Dept Pathol & Immunol, St Louis, MO 63110 USA

[6] Midw Reg Ctr Excellence Biodef & Emerging Infect, St Louis, MO 63110 USA

来源：

NATURE | 2011年 / 469卷 / 7330期

基金：

美国国家卫生研究院;

关键词：

GENOME-WIDE ASSOCIATION; SUSCEPTIBILITY LOCI; GENE ATG16L1; CELL-DEATH; INNATE; PROTEIN; ANTIGEN; STRESS; VIRUS; PATHWAY;

D O I：

10.1038/nature09782

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Autophagy is an essential, homeostatic process by which cells break down their own components. Perhaps the most primordial function of this lysosomal degradation pathway is adaptation to nutrient deprivation. However, in complex multicellular organisms, the core molecular machinery of autophagy - the 'autophagy proteins' - orchestrates diverse aspects of cellular and organismal responses to other dangerous stimuli such as infection. Recent developments reveal a crucial role for the autophagy pathway and proteins in immunity and inflammation. They balance the beneficial and detrimental effects of immunity and inflammation, and thereby may protect against infectious, autoimmune and inflammatory diseases.

引用

页码：323 / 335

页数：13

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