JunB is required for CD8+ T cell responses to acute infections.

IF 4.8 4区 医学 Q2 IMMUNOLOGY
Shukla Sarkar, Naoyuki Taira, Tsung-Han Hsieh, Hsiao-Chiao Chien, Masato Hirota, Shin-Ichi Koizumi, Daiki Sasaki, Miho Tamai, Yu Seto, Mio Miyagi, Hiroki Ishikawa
{"title":"JunB is required for CD8+ T cell responses to acute infections.","authors":"Shukla Sarkar, Naoyuki Taira, Tsung-Han Hsieh, Hsiao-Chiao Chien, Masato Hirota, Shin-Ichi Koizumi, Daiki Sasaki, Miho Tamai, Yu Seto, Mio Miyagi, Hiroki Ishikawa","doi":"10.1093/intimm/dxae063","DOIUrl":null,"url":null,"abstract":"<p><p>Basic-leucine zipper transcription factor ATF-like (BATF) and interferon regulatory factor 4 (IRF4) are crucial transcription factors for generation of cytotoxic effector and memory CD8+ T cells. JunB is required for expression of genes controlled by BATF and IRF4 in CD4+ T cell responses, but the role of JunB in CD8+ T cells remains unknown. Here, we demonstrate that JunB is essential for cytotoxic CD8+ T cell responses. JunB expression is transiently induced, depending on T cell receptor (TCR) signal strength. JunB deficiency severely impairs clonal expansion of effector CD8+ T cells in response to acute infection with Listeria monocytogenes. Junb-deficient CD8+ T cells fail to control transcription and chromatin accessibility of a specific set of genes regulated by BATF and IRF4, resulting in impaired cell survival, glycolysis, and cytotoxic CD8+ T cell differentiation. Furthermore, JunB deficiency enhances expression of coinhibitory receptors, including programmed death receptor 1 (PD-1) and T-cell immunoglobulin mucin-3 (TIM3) upon activation of naïve CD8+ T cells. These results indicate that JunB, in collaboration with BATF and IRF4, promotes multiple key events in the early stage of cytotoxic CD8+ T cell responses.</p>","PeriodicalId":13743,"journal":{"name":"International immunology","volume":null,"pages":null},"PeriodicalIF":4.8000,"publicationDate":"2024-10-19","publicationTypes":"Journal Article","fieldsOfStudy":null,"isOpenAccess":false,"openAccessPdf":"","citationCount":"0","resultStr":null,"platform":"Semanticscholar","paperid":null,"PeriodicalName":"International immunology","FirstCategoryId":"3","ListUrlMain":"https://doi.org/10.1093/intimm/dxae063","RegionNum":4,"RegionCategory":"医学","ArticlePicture":[],"TitleCN":null,"AbstractTextCN":null,"PMCID":null,"EPubDate":"","PubModel":"","JCR":"Q2","JCRName":"IMMUNOLOGY","Score":null,"Total":0}
引用次数: 0

Abstract

Basic-leucine zipper transcription factor ATF-like (BATF) and interferon regulatory factor 4 (IRF4) are crucial transcription factors for generation of cytotoxic effector and memory CD8+ T cells. JunB is required for expression of genes controlled by BATF and IRF4 in CD4+ T cell responses, but the role of JunB in CD8+ T cells remains unknown. Here, we demonstrate that JunB is essential for cytotoxic CD8+ T cell responses. JunB expression is transiently induced, depending on T cell receptor (TCR) signal strength. JunB deficiency severely impairs clonal expansion of effector CD8+ T cells in response to acute infection with Listeria monocytogenes. Junb-deficient CD8+ T cells fail to control transcription and chromatin accessibility of a specific set of genes regulated by BATF and IRF4, resulting in impaired cell survival, glycolysis, and cytotoxic CD8+ T cell differentiation. Furthermore, JunB deficiency enhances expression of coinhibitory receptors, including programmed death receptor 1 (PD-1) and T-cell immunoglobulin mucin-3 (TIM3) upon activation of naïve CD8+ T cells. These results indicate that JunB, in collaboration with BATF and IRF4, promotes multiple key events in the early stage of cytotoxic CD8+ T cell responses.

CD8+ T 细胞对急性感染的反应需要 JunB。
碱性亮氨酸拉链转录因子 ATF 样(BATF)和干扰素调节因子 4(IRF4)是产生细胞毒性效应细胞和记忆 CD8+ T 细胞的关键转录因子。在 CD4+ T 细胞反应中,由 BATF 和 IRF4 控制的基因的表达需要 JunB,但 JunB 在 CD8+ T 细胞中的作用仍然未知。在这里,我们证明了 JunB 对于细胞毒性 CD8+ T 细胞反应至关重要。JunB的表达是瞬时诱导的,取决于T细胞受体(TCR)的信号强度。在李斯特菌急性感染时,缺乏JunB会严重影响效应CD8+ T细胞的克隆扩增。Junb缺陷的CD8+ T细胞无法控制由BATF和IRF4调控的一组特定基因的转录和染色质可及性,导致细胞存活、糖酵解和细胞毒性CD8+ T细胞分化受损。此外,在激活幼稚 CD8+ T 细胞时,缺乏 JunB 会增强共抑制受体的表达,包括程序性死亡受体 1(PD-1)和 T 细胞免疫球蛋白粘蛋白-3(TIM3)。这些结果表明,JunB 与 BATF 和 IRF4 合作,促进了细胞毒性 CD8+ T 细胞反应早期的多个关键事件。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
求助全文
约1分钟内获得全文 求助全文
来源期刊
International immunology
International immunology 医学-免疫学
CiteScore
9.30
自引率
2.30%
发文量
51
审稿时长
6-12 weeks
期刊介绍: International Immunology is an online only (from Jan 2018) journal that publishes basic research and clinical studies from all areas of immunology and includes research conducted in laboratories throughout the world.
×
引用
GB/T 7714-2015
复制
MLA
复制
APA
复制
导出至
BibTeX EndNote RefMan NoteFirst NoteExpress
×
提示
您的信息不完整,为了账户安全,请先补充。
现在去补充
×
提示
您因"违规操作"
具体请查看互助需知
我知道了
×
提示
确定
请完成安全验证×
copy
已复制链接
快去分享给好友吧!
我知道了
右上角分享
点击右上角分享
0
联系我们:info@booksci.cn Book学术提供免费学术资源搜索服务,方便国内外学者检索中英文文献。致力于提供最便捷和优质的服务体验。 Copyright © 2023 布克学术 All rights reserved.
京ICP备2023020795号-1
ghs 京公网安备 11010802042870号
Book学术文献互助
Book学术文献互助群
群 号:481959085
Book学术官方微信