加州大学Ananda W. Goldrath小组的一项最新研究的论文发现了不同的组织微环境促进了前列腺组织驻留记忆CD8⁺ T细胞的分化和异质性。2026年4月1日出版的《免疫学》发表了这项成果。

课题组发现，在小鼠急性感染后，前列腺中形成了一个保护性的、异质性的、长寿命的、组织驻留的记忆性CD8⁺ T （Trm）细胞池。前列腺Trm细胞随时间的分化特征，结合TGFβ、IL-7和IL-15信号的功能询问，揭示了小鼠和人类不同前列腺基质和腺上皮小生境产生的小生境依赖的表型和功能多样性。例如，促Trm细胞因子IL-15和TGFβ在前列腺上皮中含量最高，其中CD8⁺ T细胞最持久，细胞毒性最强，并为Trm分子程序富集。总之，该课题组研究人员为前列腺Trm细胞分化提供了一个空间框架，绘制了通过局部信号的动态调节影响T细胞命运的离散组织区域。

据介绍，前列腺是一个重要的外分泌器官，是男性生殖系统的屏障组织，也是恶性肿瘤的常见部位，但前列腺中的CD8⁺ T细胞在很大程度上仍未被表征。

附：英文原文

Title: Distinct tissue niches contribute to prostate tissue-resident memory CD8+ T cell differentiation and heterogeneity

Author: Kennidy K. Takehara, Alexander Monell, Vida Luna, Baxter Melisso, Kianoosh M. Mempel, Kitty P. Cheung, Natalie Zane, Peter P. Challita, Amir Ferry, Ethan C. Xu, Violante Olivari, Nicole E. Scharping, Giovanni Galletti, Sara Quon, Julien R. Ishibashi, Nina Estep, John B. Johanneson, Chinmayi Pandya, Stephanie D. Anover-Sombke, Rana R. McKay, Peter J. Skene, Matthew E. Pipkin, Maximilian Heeg, Miguel Reina-Campos, Ananda W. Goldrath

Issue&Volume: 2026-04-01

Abstract: The prostate is an important exocrine organ, a barrier tissue of the male reproductive system, and a common site of malignancy, yet CD8+ T cells in the prostate remain largely uncharacterized. Here, we show that a protective, heterogeneous pool of long-lived, tissue-resident memory CD8+ T (Trm) cells forms in the prostate following acute infection in mice. Characterization of prostate Trm cell differentiation over time, combined with functional interrogation of TGFβ, IL-7, and IL-15 signaling, revealed niche-dependent phenotypic and functional diversity arising from distinct prostate stromal and glandular epithelial niches in both mice and humans. For instance, the Trm-promoting cytokines IL-15 and TGFβ were highest in the prostate epithelium, where CD8+ T cells were most persistent, cytotoxic, and enriched for the Trm molecular program. In sum, we provide a spatial framework for prostate Trm cell differentiation, charting the discrete tissue regions that influence T cell fate through dynamic regulation of localized signals.

DOI: 10.1016/j.immuni.2026.03.003

Source: https://www.cell.com/immunity/abstract/S1074-7613(26)00114-7