Roles of Endoplasmic Reticulum Stress in Immune Responses
Jae-Seon So*
Department of Medical Biotechnology, Dongguk University Gyeongju, Gyeongju 38066, Korea
*Correspondence: sojs@dongguk.ac.kr
Received May 29, 2018; Revised July 3, 2018; Accepted July 19, 2018.; Published online July 30, 2018.
© Korean Society for Molecular and Cellular Biology. All rights reserved.

This is an open-access article distributed under the terms of the Creative Commons Attribution-NonCommercial-ShareAlike 3.0 Unported License. To view a copy of this license, visit (http://creativecommons.org/licenses/by-nc-sa/3.0/).
ABSTRACT
The endoplasmic reticulum (ER) is a critical organelle for protein synthesis, folding and modification, and lipid synthesis and calcium storage. Dysregulation of ER functions leads to the accumulation of misfolded- or unfolded-protein in the ER lumen, and this triggers the unfolded protein response (UPR), which restores ER homeostasis. The UPR is characterized by three distinct downstream signaling pathways that promote cell survival or apoptosis depending on the stressor, the intensity and duration of ER stress, and the cell type. Mammalian cells express the UPR transducers IRE1, PERK, and ATF6, which control transcriptional and translational responses to ER stress. Direct links between ER stress and immune responses are also evident, but the mechanisms by which UPR signaling cascades are coordinated with immunity remain unclear. This review discusses recent investigations of the roles of ER stress in immune responses that lead to differentiation, maturation, and cytokine expression in immune cells. Further understanding of how ER stress contributes to the pathogenesis of immune disorders will facilitate the development of novel therapies that target UPR pathways.
Keywords: ER stress, immune response, inositol requiring enzyme 1 (IRE1), unfolded protein response (UPR), X-box binding protein 1 (XBP1)


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31 July 2018 Volume 41,
Number 7, pp. 613~703

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