Regulated activation of the cytokine TGF-β by integrins αvβ6 and αvβ8 expressed on keratinocytes is required for residence of epidermal-resident memory T cells, but whether skin-derived signals also affect recirculating memory cells in the skin remains unclear. Here, we show that after resolution of skin vaccinia virus (VV) infection, antigen-specific circulating memory CD8+ T cells migrated into skin. In mice lacking αvβ6 and αvβ8 integrins (Itgb6-/-Itgb8fl/fl-K14-cre), the absence of epidermal-activated TGF-β resulted in a gradual loss of E- or P-selectin-binding central and peripheral memory populations, which were rescued when skin entry was inhibited. Skin recirculating memory cells were required for optimal host defense against skin VV infection. These data demonstrate that skin migration can persist after resolution of local skin infection and that the cytokine environment within this nonlymphoid tissue shapes the differentiation state and persistence of the central and peripheral memory-T-cell pool.

中文翻译：

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角质形成细胞介导的细胞因子 TGF-β 激活维持皮肤循环记忆 CD8+ T 细胞。

表皮驻留记忆 T 细胞的驻留需要角质形成细胞上表达的整合素 αvβ6 和 αvβ8 对细胞因子 TGF-β 的调节激活，但皮肤来源的信号是否也会影响皮肤中的再循环记忆细胞仍不清楚。在这里，我们表明，在解决皮肤痘苗病毒 (VV) 感染后，抗原特异性循环记忆 CD8+ T 细胞迁移到皮肤中。在缺乏 αvβ6 和 αvβ8 整合素 (Itgb6-/-Itgb8fl/fl-K14-cre) 的小鼠中，表皮激活的 TGF-β 的缺失导致 E-或 P-选择素结合的中枢和外周记忆群体逐渐丧失，当皮肤进入被抑制时获救。皮肤再循环记忆细胞是针对皮肤 VV 感染的最佳宿主防御所必需的。