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CD7在慢性感染期间调节终末耗竭CD8 T细胞的持久性。

CD7 regulates the persistence of terminally exhausted CD8 T cells during chronic infection.

作者信息

Hyslop Sean, Hofferek Colby J, Stegantseva Maria V, Kan Emerald, McCord Kelli A, Alvarez Victor M, Xia Amanda Y, Conarty Jacob P, Wieland Andreas, Hudson William H

机构信息

Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA; Medical Scientist Training Program, Baylor College of Medicine, Houston, TX 77030, USA.

Department of Molecular and Cellular Biology, Baylor College of Medicine, Houston, TX 77030, USA.

出版信息

Cell Rep. 2025 Sep 18;44(10):116316. doi: 10.1016/j.celrep.2025.116316.

DOI:10.1016/j.celrep.2025.116316
PMID:40974572
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12509300/
Abstract

CD8 T cell exhaustion limits immune responses during cancer and chronic infection. We identify CD7 as a tissue-specific regulator of terminally exhausted CD8 T cells during chronic infection. CD7 expression progressively increases during exhaustion, reaching its highest levels on a subset of CD101Tim3 terminally exhausted cells that arise in the liver. Transcriptomic analysis revealed that CD7-deficient terminally exhausted cells display altered expression of co-stimulatory, translational, and effector genes, correlating with markedly reduced persistence and increased apoptotic susceptibility. Importantly, CD7 is preferentially upregulated on PD-1CD39 tumor-infiltrating lymphocytes in human head and neck squamous cell carcinoma, suggesting that CD7 may play a conserved role in promoting exhausted T cell survival. These findings reveal a function for CD7 in sustaining terminally exhausted CD8 T cells and demonstrate that CD7 signaling is a critical regulator of T cell persistence during chronic infection.

摘要

CD8 T细胞耗竭会限制癌症和慢性感染期间的免疫反应。我们确定CD7是慢性感染期间终末耗竭CD8 T细胞的组织特异性调节因子。在耗竭过程中，CD7表达逐渐增加，在肝脏中出现的CD101Tim3终末耗竭细胞亚群上达到最高水平。转录组分析显示，缺乏CD7的终末耗竭细胞共刺激、翻译和效应基因的表达发生改变，这与持久性显著降低和凋亡易感性增加相关。重要的是，在人头颈部鳞状细胞癌的PD-1CD39肿瘤浸润淋巴细胞上，CD7优先上调，这表明CD7可能在促进耗竭T细胞存活中发挥保守作用。这些发现揭示了CD7在维持终末耗竭CD8 T细胞中的作用，并证明CD7信号是慢性感染期间T细胞持久性的关键调节因子。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9615/12509300/4f3156733d9a/nihms-2112853-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9615/12509300/452ab7ec6cb7/nihms-2112853-f0001.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9615/12509300/270f5e17d831/nihms-2112853-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9615/12509300/a2307d8267bb/nihms-2112853-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9615/12509300/4f3156733d9a/nihms-2112853-f0007.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9615/12509300/452ab7ec6cb7/nihms-2112853-f0001.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9615/12509300/312ebf7c8fc5/nihms-2112853-f0002.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9615/12509300/f63f13e23f98/nihms-2112853-f0003.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9615/12509300/ca98f1fb9c3e/nihms-2112853-f0004.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9615/12509300/270f5e17d831/nihms-2112853-f0005.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9615/12509300/a2307d8267bb/nihms-2112853-f0006.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/9615/12509300/4f3156733d9a/nihms-2112853-f0007.jpg

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本文引用的文献

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An early precursor CD8 T cell that adapts to acute or chronic viral infection.一种适应急性或慢性病毒感染的早期前体CD8 T细胞。
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Precursors of exhausted T cells are pre-emptively formed in acute infection.耗竭性T细胞的前体在急性感染中预先形成。
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LAG-3 and PD-1 synergize on CD8 T cells to drive T cell exhaustion and hinder autocrine IFN-γ-dependent anti-tumor immunity.
LAG-3 和 PD-1 在 CD8 T 细胞上协同作用，导致 T 细胞耗竭，并阻碍自分泌 IFN-γ 依赖的抗肿瘤免疫。
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