抗原衍生肽参与内质网应激传感器IRE1α抑制树突状细胞交叉呈递

The Journal of Cell Biology Pub Date : 2022-04-21 DOI:10.1083/jcb.202111068

Ofer Guttman, Adrien Le Thomas, S. Marsters, D. Lawrence, Lauren M. Gutgesell, Iratxe Zuazo-Gaztelu, J. Harnoss, S. M. Haag, A. Murthy, G. Strasser, Z. Modrušan, Thomas Wu, I. Mellman, A. Ashkenazi

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引用次数: 13

摘要

抗原交叉呈递树突状细胞(dc)在没有内质网应激的情况下激活内质网应激传感器IRE1α。Guttman等人的研究表明，抗原来源的er导入肽可以直接作用于IRE1α。IRE1α依赖的MHC-I mRNA衰减抑制DC交叉呈递，而IRE1α抑制增强抗肿瘤免疫。

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Antigen-derived peptides engage the ER stress sensor IRE1α to curb dendritic cell cross-presentation

Antigen cross-presenting dendritic cells (DCs) activate the ER stress sensor IRE1α without ER stress. Guttman et al. show that antigen-derived ER-imported peptides can directly engage IRE1α. Regulated IRE1α-dependent MHC-I mRNA decay curbs DC cross-presentation, while IRE1α inhibition augments antitumor immunity.

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The Journal of Cell Biology

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