Ms4a7 expression in cDC1s determines cross-presentation and antitumor immunity

• 成果类型: Article
• 署名作者: Xie, Bowen; Yuan, Bowen; Zhao, Xiaohong; Xie, Tian; Li, Ruifeng; Wei, Peng; Sun, Qinli; Hu, Wenbo; Pan, Birui; Chen, Yongzhen; Wei, Kun; Zhao, Zixuan; Yuan, Lei; Zhong, Xuan; Bai, Xue; Lan, Qiuyan; Qin, Lei; Ni, Ling; Dong, Chen
• 署名单位: Westlake University; Tsinghua University; Tsinghua University; Tsinghua University; Central South University
• 刊物名称: SCIENCE
• ISSN/ISSBN: 0036-8075; 1095-9203
• DOI: 10.1126/science.ady5362
• 发表日期: 2025-11-13
• 页码: eady5362
• 关键词: DENDRITIC CELL-RECEPTOR; f-actin; pd-1 blockade; antigen; cd8(+); reveals; murine; FAMILY; DNGR-1; TRAFFICKING

摘要

Conventional type 1 dendritic cells (cDC1s) capture antigens in peripheral tissues and migrate to draining lymph nodes (dLNs) to prime antigen-specific CD8+ T cells. How tumor antigens are processed to activate CD8+ T cell immunity is not well understood. In this work, we show that Ms4a7 is up-regulated in cDC1s after tumor antigen uptake or exposure to exogenous stimuli and is required for their cross-priming ability. Although Ms4a7-/- mice showed normal cDC1 development and turnover, they failed to prime antigen-specific CD8+ T cells following infection or tumor development. In human cancers, MS4A7 was expressed in a subset of cDC1s, preferentially enriched in dLNs, and correlated with patient survival. Our findings suggest a critical role for Ms4a7 in cDC1-mediated cross-presentation and antitumor CD8+ T cell responses.