美国国立卫生研究院Jung-Hyun Park小组的研究认为整合素CD103在初始CD8⁺ T细胞中的表达促进细胞因子驱动的记忆表型和效应功能的获得。相关论文发表在2025年9月15日出版的《免疫学》杂志上。

课题组报道了CD103在初始CD8⁺ T细胞中的表达促进了它们与E-cadherin表达细胞的结合，促进了它们获得记忆表型和效应功能。值得注意的是，表达E-cadherin并产生I型干扰素和白细胞介素-12（IL-12）的树突状细胞（DC）亚群负责这一过程。因此，DC特异性E-cadherin的缺失导致效应CD8⁺ T细胞分化减少，肿瘤易感性增加，而CD103的强制表达增强了CD8⁺ T细胞的效应功能和抗肿瘤活性，揭示了CD103在细胞毒性T细胞免疫中的调节作用。

据了解，整合素CD103结合E-cadherin， E-cadherin是一种主要表达于上皮细胞的细胞粘附分子，它们介导CD103⁺ T细胞在屏障部位的组织驻留。重要的是，循环的初始CD8⁺ T细胞也表达大量的CD103，但CD103是否有助于CD8⁺ T细胞免疫，而不仅仅是在细胞粘附中的作用尚不清楚。

附：英文原文

Title: Integrin CD103 expression in naive CD8+ T cells promotes cytokine-driven acquisition of memory phenotype and effector function

Author: Can Li, Davinna L. Ligons, Dominic Lanasa, Hilary R. Keller, Megan A. Luckey, Brian Capaldo, Daoud Meerzaman, Joo-Young Park, Jung-Hyun Park

Issue&Volume: 2025-09-15

Abstract: Integrin CD103 binds to E-cadherin, a cell adhesion molecule predominantly expressed on epithelial cells, thus mediating the tissue residency of CD103+ T cells in barrier sites. Importantly, circulating naive CD8+ T cells also express large amounts of CD103, but whether CD103 contributes to CD8+ T cell immunity beyond its role in cell adhesion is unclear. Here, we report that CD103 expression in naive CD8+ T cells facilitates their engagement with E-cadherin-expressing cells, promoting their acquisition of memory phenotype and effector function. Notably, dendritic cell (DC) subsets expressing E-cadherin and producing type I interferons and interleukin-12 (IL-12) were responsible for this process. As a corollary, the DC-specific loss of E-cadherin resulted in diminished effector CD8+ T cell differentiation and increased tumor susceptibility, while the forced expression of CD103 enhanced the effector functions and anti-tumor activity of CD8+ T cells, revealing a regulatory role for CD103 in cytotoxic T cell immunity.

DOI: 10.1016/j.immuni.2025.08.014

Source: https://www.cell.com/immunity/abstract/S1074-7613(25)00377-2