转录调节因子 ID3 在肿瘤发生过程中维持引流淋巴结中的肿瘤特异性记忆 CD8 T 细胞。
The transcription regulator ID3 maintains tumor-specific memory CD8+ T cells in draining lymph nodes during tumorigenesis.
发表日期：2024 Aug 30
作者：
Ling Ran, Zhengliang Yue, Mengqu Ran, Qiao Liu, Xingxing Su, Lisha Wang, Shuqiong Wen, Luming Xu, Shun Lei, Zhanpeng Ou, Jianjun Hu, Yan Zhang, Chenxi Qin, Yuzhu Wang, Qinyi He, Yezi Chen, Wen Liu, Lilin Ye, Qizhao Huang, Lifan Xu
来源：
Cell Reports
摘要：
在肿瘤发生过程中，最近在引流淋巴结中发现的肿瘤特异性记忆 T 细胞（TdLN-TTSM 细胞）在肿瘤抑制中发挥着关键作用，可产生祖细胞耗竭 T (TPEX) 细胞，并进一步补充驻留的肿瘤特异性 CD8 T 细胞在肿瘤微环境（TME）中。然而，TTSM 细胞如何在 TdLN 中维持尚不清楚。在这里，我们发现与其他 CD8 T 细胞亚群相比，TTSM 细胞高度表达转录调节因子 ID3（DNA 结合抑制剂 3）。 ID3 的缺乏会显着干扰 TTSM 和 TPEX 细胞的维持，导致肿瘤浸润 CD8 T 细胞减少并损害肿瘤控制。与此一致的是，CD8 T 细胞中 ID3 的过度表达会增加 TTSM 细胞数量并增强抗肿瘤免疫反应。版权所有 © 2024 作者。由爱思唯尔公司出版。保留所有权利。
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.