• 文献检索
  • 文档翻译
  • 深度研究
  • 学术资讯
  • Suppr Zotero 插件Zotero 插件
  • 邀请有礼
  • 套餐&价格
  • 历史记录
应用&插件
Suppr Zotero 插件Zotero 插件浏览器插件Mac 客户端Windows 客户端微信小程序
定价
高级版会员购买积分包购买API积分包
服务
文献检索文档翻译深度研究API 文档MCP 服务
关于我们
关于 Suppr公司介绍联系我们用户协议隐私条款
关注我们

Suppr 超能文献

核心技术专利:CN118964589B侵权必究
粤ICP备2023148730 号-1Suppr @ 2026

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验

颠覆肿瘤免疫治疗:释放衰竭祖细胞 T 细胞的潜能。

Revolutionizing tumor immunotherapy: unleashing the power of progenitor exhausted T cells.

机构信息

Department of Tumor Biological Treatment, The Third Affiliated Hospital of Soochow University, Changzhou 213003, China.

Jiangsu Engineering Research Center for Tumor Immunotherapy, The Third Affiliated Hospital of Soochow University, Changzhou 213003, China.

出版信息

Cancer Biol Med. 2024 May 31;21(6):499-512. doi: 10.20892/j.issn.2095-3941.2024.0105.

DOI:10.20892/j.issn.2095-3941.2024.0105
PMID:38825813
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11208905/
Abstract

In exploring persistent infections and malignancies, a distinctive subgroup of CD8 T cells, progenitor exhausted CD8 T (Tpex) cells, has been identified. These Tpex cells are notable for their remarkable self-renewal and rapid proliferation abilities. Recent strides in immunotherapy have demonstrated that Tpex cells expand and differentiate into responsive exhausted CD8 T cells, thus underscoring their critical role in the immunotherapeutic retort. Clinical examinations have further clarified a robust positive correlation between the proportional abundance of Tpex cells and enhanced clinical prognosis. Tpex cells have found noteworthy applications in the formulation of inventive immunotherapeutic approaches against tumors. This review describes the functions of Tpex cells in the tumor milieu, particularly their potential utility in tumor immunotherapy. Precisely directing Tpex cells may be essential to achieving successful outcomes in immunotherapy against tumors.

摘要

在探索持续性感染和恶性肿瘤的过程中,人们发现了一组独特的 CD8 T 细胞亚群,即前体细胞耗竭 CD8 T(Tpex)细胞。这些 Tpex 细胞的显著特点是具有很强的自我更新和快速增殖能力。最近的免疫治疗进展表明,Tpex 细胞可以扩增并分化为有反应性的耗竭 CD8 T 细胞,这突出了它们在免疫治疗反应中的关键作用。临床检查进一步明确了 Tpex 细胞的比例丰度与增强的临床预后之间存在强烈的正相关关系。Tpex 细胞在肿瘤创新性免疫治疗方法的制定中得到了广泛的应用。本综述描述了 Tpex 细胞在肿瘤微环境中的功能,特别是它们在肿瘤免疫治疗中的潜在应用。精确调控 Tpex 细胞可能是实现肿瘤免疫治疗成功的关键。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19d4/11208905/157511367dd7/cbm-21-499-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19d4/11208905/82aee5523bff/cbm-21-499-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19d4/11208905/1d66b1355aa5/cbm-21-499-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19d4/11208905/db62ddcfce91/cbm-21-499-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19d4/11208905/157511367dd7/cbm-21-499-g004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19d4/11208905/82aee5523bff/cbm-21-499-g001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19d4/11208905/1d66b1355aa5/cbm-21-499-g002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19d4/11208905/db62ddcfce91/cbm-21-499-g003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/19d4/11208905/157511367dd7/cbm-21-499-g004.jpg

相似文献

1
Revolutionizing tumor immunotherapy: unleashing the power of progenitor exhausted T cells.颠覆肿瘤免疫治疗:释放衰竭祖细胞 T 细胞的潜能。
Cancer Biol Med. 2024 May 31;21(6):499-512. doi: 10.20892/j.issn.2095-3941.2024.0105.
2
Precursor exhausted CD8T cells in colorectal cancer tissues associated with patient's survival and immunotherapy responsiveness.结直肠癌组织中耗尽的前体细胞 CD8T 细胞与患者的生存和免疫治疗反应相关。
Front Immunol. 2024 Mar 6;15:1362140. doi: 10.3389/fimmu.2024.1362140. eCollection 2024.
3
IL-15 promotes self-renewal of progenitor exhausted CD8 T cells during persistent antigenic stimulation.IL-15 促进持续性抗原刺激期间耗尽的祖细胞 CD8 T 细胞的自我更新。
Front Immunol. 2023 Jun 20;14:1117092. doi: 10.3389/fimmu.2023.1117092. eCollection 2023.
4
Potential mechanisms of cancer stem-like progenitor T-cell bio-behaviours.癌症干细胞样祖细胞 T 细胞生物行为的潜在机制。
Clin Transl Med. 2024 Aug;14(8):e1817. doi: 10.1002/ctm2.1817.
5
NR4A1 transcriptionally regulates the differentiation of stem-like CD8 T cells in the tumor microenvironment.NR4A1 转录调控肿瘤微环境中干细胞样 CD8 T 细胞的分化。
Cell Rep. 2024 Jun 25;43(6):114301. doi: 10.1016/j.celrep.2024.114301. Epub 2024 May 31.
6
Combining an Alarmin HMGN1 Peptide with PD-L1 Blockade Results in Robust Antitumor Effects with a Concomitant Increase of Stem-Like/Progenitor Exhausted CD8 T Cells.将警报素 HMGN1 肽与 PD-L1 阻断联合使用可产生强大的抗肿瘤作用,并同时增加干性/祖细胞耗竭的 CD8 T 细胞。
Cancer Immunol Res. 2021 Oct;9(10):1214-1228. doi: 10.1158/2326-6066.CIR-21-0265. Epub 2021 Aug 3.
7
Exhausted CD8+T Cells in the Tumor Immune Microenvironment: New Pathways to Therapy.肿瘤免疫微环境中耗竭的CD8 + T细胞:新的治疗途径
Front Immunol. 2021 Feb 2;11:622509. doi: 10.3389/fimmu.2020.622509. eCollection 2020.
8
Dynamic CD8 T cell responses to cancer immunotherapy in human regional lymph nodes are disrupted in metastatic lymph nodes.在转移性淋巴结中,癌症免疫治疗在人体区域淋巴结中诱导的动态 CD8 T 细胞反应被打乱。
Cell. 2023 Mar 16;186(6):1127-1143.e18. doi: 10.1016/j.cell.2023.02.021.
9
Antitumor progenitor exhausted CD8 T cells are sustained by TCR engagement.肿瘤杀伤祖细胞耗竭的 CD8 T 细胞受 TCR 结合维持。
Nat Immunol. 2024 Jun;25(6):1046-1058. doi: 10.1038/s41590-024-01843-8. Epub 2024 May 30.
10
Type 1 conventional dendritic cells maintain and guide the differentiation of precursors of exhausted T cells in distinct cellular niches.1 型传统树突状细胞在不同的细胞龛中维持和指导衰竭 T 细胞前体的分化。
Immunity. 2022 Apr 12;55(4):656-670.e8. doi: 10.1016/j.immuni.2022.03.006. Epub 2022 Apr 1.

引用本文的文献

1
Immune microenvironment of tumor-draining lymph nodes: insights for immunotherapy.肿瘤引流淋巴结的免疫微环境:免疫治疗的见解
Front Immunol. 2025 Apr 11;16:1562797. doi: 10.3389/fimmu.2025.1562797. eCollection 2025.
2
Aging impairs CD8 T cell responses in adoptive T-cell therapy against solid tumors.衰老会削弱过继性T细胞疗法中CD8 T细胞对实体瘤的反应。
Front Immunol. 2025 Jan 24;16:1484303. doi: 10.3389/fimmu.2025.1484303. eCollection 2025.
3
Systematic analysis of human colorectal cancer scRNA-seq revealed limited pro-tumoral IL-17 production potential in gamma delta T cells.
系统分析人类结直肠癌 scRNA-seq 揭示了 γδ T 细胞中有限的促肿瘤 IL-17 产生潜力。
Neoplasia. 2024 Dec;58:101072. doi: 10.1016/j.neo.2024.101072. Epub 2024 Oct 24.