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The transcription regulator ID3 maintains tumor-specific memory CD8+ T cells in draining lymph nodes during tumorigenesis

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资源类型：
Pubmed体系：
作者：
Ran Ling[1] * ; Yue Zhengliang[1] * ; Ran Mengqu[2] * ; Liu Qiao[3] ; Su Xingxing[1] ; Wang Lisha[1] ; Wen Shuqiong[4] ; Xu Luming[5] ; Lei Shun[1] ; Ou Zhanpeng[4] ; Hu Jianjun[1] ; Zhang Yan[2,6] ; Qin Chenxi[1] ; Wang Yuzhu[1] ; He Qinyi[1] ; Chen Yezi[2] ; Liu Wen[2] ; Ye Lilin[1] ; Huang Qizhao[2] ; Xu Lifan[1] ;
机构： [1]Institute of Immunology, Third Military Medical University, Chongqing, China [2]Institute of Immunological Innovation and Translation, Chongqing Medical University, Chongqing, China [3]Division of Pediatric Pulmonology and Immunology, West China Second University Hospital, Sichuan University, Chengdu, China [4]Stomatological Hospital of Chongqing Medical University, Chongqing, China [5]Medical Laboratory Technology, Southern Medical University, Guangzhou, China [6]Key Laboratory of Major Brain Disease and Aging Research (Ministry of Education), Chongqing Medical University, Chongqing, China
出处：
DOI： 10.1016/j.celrep.2024.114690

摘要：
During tumorigenesis, the recently identified tumor-specific memory T cells in draining lymph nodes (TdLN-TTSM cells) play a pivotal role in tumor repression that gives rise to progenitor exhausted T (TPEX) cells and further replenishes tumor-specific CD8+ T cells residing in the tumor microenvironment (TME). However, how TTSM cells are maintained in TdLN is largely unknown. Here, we show that the transcription regulator ID3 (inhibitor of DNA binding 3) is highly expressed by TTSM cells compared with other CD8+ T cell subsets. The deficiency of ID3 significantly interrupts the maintenance of TTSM and TPEX cells, resulting in decreased tumor-infiltrating CD8+ T cells and impaired tumor control. Consistent with this, overexpression of ID3 in CD8+ T cells increases the TTSM cell population and enhances the anti-tumor immune response.Copyright © 2024 The Author(s). Published by Elsevier Inc. All rights reserved.

基金：
This project was supported by grants from the National Natural Science Foundation for Outstanding Young Scholars of China (no. 82122028 to L. Xu, and no. 82322031 to Q. Huang), the National Natural Science Found for Distinguished Young Scholars of China (no. 32425002 to L.Y.), the National Natural Science Foundation of China (no. 82173094 to L. Xu), the Natural Science Foundation for Outstanding Young Scholars of Chongqing (no. CSTB2022NSCQ-JQX0015 to L. Xu, and no. CSTB2024NSCQ-JQX0008 to Q. Huang), the Natural Science Foundation of Chongqing (no. CSTB2023NSCQ-LZX0010 to Q. Huang), and the National Natural Science Foundation of China (no. 82371844 to Q.L.). We thank C.Y. Li and Y.J. Zhang from the Clinical Medical Research Center of Southwest Hospital, Third Military Medical University, for cell sorting and analysis.
语种：
外文
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出版当年[2024]版：
无
最新[2023]版：
大类 | 1 区 生物学
小类 | 2 区 细胞生物学
第一作者：
第一作者机构： [1]Institute of Immunology, Third Military Medical University, Chongqing, China
共同第一作者：
通讯作者：
推荐引用方式(GB/T 7714)：
Ran Ling,Yue Zhengliang,Ran Mengqu,et al.The transcription regulator ID3 maintains tumor-specific memory CD8+ T cells in draining lymph nodes during tumorigenesis[J].Cell Reports.2024,43(9):114690.doi:10.1016/j.celrep.2024.114690.
APA：
Ran Ling,Yue Zhengliang,Ran Mengqu,Liu Qiao,Su Xingxing...&Xu Lifan.(2024).The transcription regulator ID3 maintains tumor-specific memory CD8+ T cells in draining lymph nodes during tumorigenesis.Cell Reports,43,(9)
MLA：
Ran Ling,et al."The transcription regulator ID3 maintains tumor-specific memory CD8+ T cells in draining lymph nodes during tumorigenesis".Cell Reports 43..9(2024):114690

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