Tissue-resident memory T (TRM) cells, functionally distinct from circulating memory T cells, have a critical role in protective immunity in tissues, are more efficacious when elicited after vaccination and yield more effective antitumor immunity, yet the signals that direct development of TRM cells are incompletely understood. Here we show that type 1 regulatory T (Treg) cells, which express the transcription factor T-bet, promote the generation of CD8+ TRM cells. The absence of T-bet-expressing type 1 Treg cells reduces the presence of TRM cells in multiple tissues and increases pathogen burden upon infectious challenge. Using infection models, we show that type 1 Treg cells are specifically recruited to local inflammatory sites via the chemokine receptor CXCR3. Close proximity with effector CD8+ T cells and Treg cell expression of integrin-β8 endows the bioavailability of transforming growth factor-β in the microenvironment, thereby promoting the generation of CD8+ TRM cells.

中文翻译：

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1型Treg细胞促进CD8 +组织驻留记忆T细胞的生成。

功能与循环记忆T细胞不同的组织驻留记忆T细胞（TRM）在组织的保护性免疫中起关键作用，在接种疫苗后引发时更为有效，并产生更有效的抗肿瘤免疫力，然而直接指导TRM发育的信号细胞尚未完全了解。在这里，我们显示了表达转录因子T-bet的1型调节性T（Treg）细胞促进了CD8 + TRM细胞的生成。表达T-bet的1型Treg细胞的缺乏减少了多种组织中TRM细胞的存在，并增加了感染后的病原体负担。使用感染模型，我们显示1型Treg细胞通过趋化因子受体CXCR3专门募集到局部炎症部位。