内质网应激对免疫细胞分泌细胞因子调节作用的研究进展  

Advances in endoplasmic reticulum stress-regulated cytokine secretion by immune cells

作　　者：徐宁 赵有祺 徐灵芝 XU Ning;ZHAO Youqi;XU Lingzhi(Key Laboratory of Immune Microenvironment and Inflammatory Disease Research in Universities of Shandong Province,School of Basic Medical Sciences,Shandong Second Medical University,Weifang 261053,China)

机构地区：[1]山东第二医科大学基础医学院,山东省高等学校免疫微环境与炎症性疾病研究特色实验室,山东潍坊261053

出　　处：《中国病理生理杂志》2025年第1期157-164,共8页Chinese Journal of Pathophysiology

基　　金：国家自然科学基金资助项目(No.81701590);山东省高等学校青创科技支持计划(No.2021KJ106)。

摘　　要：分泌性蛋白的合成、加工和运输是在内质网腔完成的,Ca^(2+)或内环境稳态的任何干扰均可导致错误折叠或未折叠蛋白的产生,进而导致内质网应激(ERS)。通过启动未折叠蛋白反应中的三条信号通路:肌醇需求酶1(IRE1)、蛋白激酶R样内质网激酶(PERK)和转录激活因子6(ATF6),ERS可维持分泌蛋白的正确折叠。细胞因子作为小分子分泌蛋白,在病毒感染、自身免疫性疾病及炎症等疾病状态下,多由活化的免疫细胞大量分泌,其分泌途径的平衡受ERS调节,进而影响细胞功能。有关ERS调节免疫细胞分泌细胞因子的确切机制尚未完全阐明。本文对ERS调节免疫细胞分泌细胞因子的作用及机制的研究进展做了综述。Within the lumen of the endoplasmic reticulum,secretory proteins are synthesized,processed,and transported.Disturbances in Ca^(2+)or internal environmental homeostasis trigger the production of misfolded or unfolded proteins,thereby inducing endoplasmic reticulum stress(ERS).The ERS maintains the correct folding of secretory proteins by activating three signaling pathways in the unfolded protein response:inositol-requiring enzyme 1(IRE1),protein kinase R-like endoplasmic reticulum kinase(PERK),and activating transcription factor 6(ATF6).In disease states such as viral infections,autoimmune diseases,and inflammation,activated immune cells secrete large amounts of cytokines,which are small molecule secretory proteins.The ERS regulates the balance of its secretory pathways,thereby affecting cellular function.The precise mechanism by which ERS affects immune cells regulating cytokine secretion remains to be fully revealed.This article provides a comprehensive review of the research progress on the role and mechanism of ERS in regulating the secretion of cytokines by immune cells.

关 键 词：内质网应激 未折叠蛋白反应 细胞因子 免疫细胞 

分 类 号：R392.32[医药卫生—免疫学] Q244[医药卫生—基础医学] R593[生物学—细胞生物学]