Endoplasmic Reticulum Stress in Immunity

被引：372

作者：

Bettigole, Sarah E. ^{[1
,2
]}

Glimcher, Laurie H. ^{[1
]}

机构：

[1] Weill Cornell Med Coll, Dept Med, New York, NY 10065 USA

[2] Harvard Univ, Sch Med, Div Med Sci, Program Immunol, Boston, MA 02115 USA

来源：

ANNUAL REVIEW OF IMMUNOLOGY VOL 33 | 2015年 / 33卷

关键词：

IRE1; XBP-1; PERK; ATF6; proteostasis; inflammation; UNFOLDED-PROTEIN-RESPONSE; PLASMA-CELL DIFFERENTIATION; NF-KAPPA-B; THIOREDOXIN-INTERACTING PROTEIN; IFN-BETA INDUCTION; ER STRESS; TRANSCRIPTION FACTOR; OXIDATIVE STRESS; MESSENGER-RNA; SUBTILASE CYTOTOXIN;

D O I：

10.1146/annurev-immunol-032414-112116

中图分类号：

R392 [医学免疫学]; Q939.91 [免疫学];

学科分类号：

100102 ;

摘要：

Immune responses occur in the midst of a variety of cellular stresses that can severely perturb endoplasmic reticulum (ER) function. The unfolded protein response is a three-pronged signaling axis dedicated to preserving ER homeostasis. In this review, we highlight many important and emerging functional roles for ER stress in immunity, focusing on how the bidirectional cross talk between immunological processes and basic cell biology leads to pleiotropic signaling outcomes and enhanced sensitivity to inflammatory stimuli. We also discuss how dysregulated ER stress responses can provoke many diseases, including autoimmunity, firmly positioning the unfolded protein response as a major therapeutic target in human disease.

引用

页码：107 / 138

页数：32

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