效应器
生物
细胞生物学
CD8型
细胞毒性T细胞
细胞分化
T细胞
白细胞介素2受体
免疫学
免疫系统
遗传学
基因
体外
作者
Anjun Jiao,Haiyan Liu,Renyi Ding,Huiqiang Zheng,Cangang Zhang,Zhao Feng,Lei Lei,Xin Wang,Yanhong Su,Xiaofeng Yang,Chenming Sun,Lianjun Zhang,Liang Bai,Lina Sun,Baojun Zhang
出处
期刊:Journal of Immunology
[The American Association of Immunologists]
日期:2022-09-01
卷期号:209 (5): 855-863
被引量:1
标识
DOI:10.4049/jimmunol.2200037
摘要
Effector CD8+ T cells are crucial players in adaptive immunity for effective protection against invading pathogens. The regulatory mechanisms underlying CD8+ T cell effector differentiation are incompletely understood. In this study, we defined a critical role of mediator complex subunit 1 (Med1) in controlling effector CD8+ T cell differentiation and survival during acute bacterial infection. Mice with Med1-deficient CD8+ T cells exhibited significantly impaired expansion with evidently reduced killer cell lectin-like receptor G1+ terminally differentiated and Ly6c+ effector cell populations. Moreover, Med1 deficiency led to enhanced cell apoptosis and expression of multiple inhibitory receptors (programmed cell death 1, T cell Ig and mucin domain-containing-3, and T cell immunoreceptor with Ig and ITIM domains). RNA-sequencing analysis revealed that T-bet- and Zeb2-mediated transcriptional programs were impaired in Med1-deficient CD8+ T cells. Overexpression of T-bet could rescue the differentiation and survival of Med1-deficient CD8+ effector T cells. Mechanistically, the transcription factor C/EBPβ promoted T-bet expression through interacting with Med1 in effector T cells. Collectively, our findings revealed a novel role of Med1 in regulating effector CD8+ T cell differentiation and survival in response to bacterial infection.
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