芳香烃受体
细胞毒性T细胞
白细胞介素-7受体
颗粒酶B
生物
细胞生物学
白细胞介素2受体
白细胞介素21
CD8型
颗粒酶
T细胞
细胞分化
化学
穿孔素
免疫学
免疫系统
转录因子
体外
遗传学
基因
作者
Joseph Dean,Eric Y. Helm,Zheng Qing Fu,Lifeng Xiong,Na Sun,Kristen N. Oliff,Marcus Muehlbauer,Dorina Avram,Liang Zhou
出处
期刊:Cell Reports
[Elsevier]
日期:2023-01-01
卷期号:42 (1): 111963-111963
被引量:13
标识
DOI:10.1016/j.celrep.2022.111963
摘要
The Aryl hydrocarbon receptor (Ahr) regulates the differentiation and function of CD4+ T cells; however, its cell-intrinsic role in CD8+ T cells remains elusive. Herein we show that Ahr acts as a promoter of resident memory CD8+ T cell (TRM) differentiation and function. Genetic ablation of Ahr in mouse CD8+ T cells leads to increased CD127–KLRG1+ short-lived effector cells and CD44+CD62L+ T central memory cells but reduced granzyme-B-producing CD69+CD103+ TRM cells. Genome-wide analyses reveal that Ahr suppresses the circulating while promoting the resident memory core gene program. A tumor resident polyfunctional CD8+ T cell population, revealed by single-cell RNA-seq, is diminished upon Ahr deletion, compromising anti-tumor immunity. Human intestinal intraepithelial CD8+ T cells also highly express AHR that regulates in vitro TRM differentiation and granzyme B production. Collectively, these data suggest that Ahr is an important cell-intrinsic factor for CD8+ T cell immunity.
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