Molecular Evaluation of Endoplasmic Reticulum Homeostasis Meets Humoral Immunity

被引：33

作者：

van Anken, Eelco ^{[1
,2
]}

Bakunts, Anush ^{[1
]}

Hu, Chih-Chi Andrew ^{[3
,6
]}

Janssens, Sophie ^{[4
,5
]}

Sitia, Roberto ^{[1
,2
]}

机构：

[1] Ist Sci San Raffaele, Div Genet & Cell Biol, Milan, Italy

[2] Univ Vita Salute San Raffaele, Milan, Italy

[3] Wistar Inst Anat & Biol, 3601 Spruce St, Philadelphia, PA 19104 USA

[4] Univ Ghent, VIB Ctr Inflammat Res, Lab Endoplasm Reticulum ER Stress & Inflammat, Ghent, Belgium

[5] Univ Ghent, Dept Internal Med & Pediat, Ghent, Belgium

[6] Houston Methodist Acad Inst, Houston Methodist Canc Ctr, Houston, TX USA

来源：

TRENDS IN CELL BIOLOGY | 2021年 / 31卷 / 07期

基金：

欧洲研究理事会;

关键词：

UNFOLDED-PROTEIN-RESPONSE; PLASMA-CELL DIFFERENTIATION; THIOREDOXIN-INTERACTING PROTEIN; ER STRESS; TRANSMEMBRANE PROTEIN; QUALITY-CONTROL; B-LYMPHOCYTES; TRANSCRIPTIONAL INDUCTION; LIGHT-CHAIN; IMMUNOGLOBULIN;

D O I：

10.1016/j.tcb.2021.02.004

中图分类号：

Q2 [细胞生物学];

学科分类号：

071009 ; 090102 ;

摘要：

The biosynthesis of about one third of the human proteome, including membrane receptors and secreted proteins, occurs in the endoplasmic reticulum (ER). Conditions that perturb ER homeostasis activate the unfolded protein response (UPR). An 'optimistic' UPR output aims at restoring homeostasis by reinforcement of machineries that guarantee efficiency and fidelity of protein biogenesis in the ER. Yet, once the UPR 'deems' that ER homeostatic readjustment fails, it transitions to a 'pessimistic' output, which, depending on the cell type, will result in apoptosis. In this article, we discuss emerging concepts on how the UPR 'evaluates' ER stress, how the UPR is repurposed, in particular in B cells, and how UPR-driven counter-selection of cells undergoing homeostatic failure serves organismal homeostasis and humoral immunity.

引用

页码：529 / 541

页数：13

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