Following antigen-driven expansion in lymph node, transforming growth factor-β (TGFβ) is required for differentiation of skin-recruited CD8⁺ T cell effectors into epidermal resident memory T (Trm) cells and their epidermal persistence. We found that the source of TGFβ -supporting Trm cells was autocrine. In addition, antigen-specific Trm cells that encountered cognate antigen in the skin, and bystander Trm cells that did not, both displayed long-term persistence in the epidermis under steady-state conditions. However, when the active-TGFβ was limited or when new T cell clones were recruited into the epidermis, antigen-specific Trm cells were more efficiently retained than bystander Trm cells. Genetically enforced TGFβR signaling allowed bystander Trm cells to persist in the epidermis as efficiently as antigen-specific Trm cells in both contexts. Thus, competition between T cells for active TGFβ represents an unappreciated selective pressure that promotes the accumulation and persistence of antigen-specific Trm cells in the epidermal niche.

在抗原驱动的淋巴结扩张后，转化生长因子-β (TGFβ) 是皮肤募集的 CD8 ^{+分化所必需的}T 细胞效应进入表皮常驻记忆 T (Trm) 细胞及其表皮持久性。我们发现支持 TGFβ 的 Trm 细胞的来源是自分泌​​。此外，在皮肤中遇到同源抗原的抗原特异性 Trm 细胞和没有遇到同源抗原的旁观者 Trm 细胞在稳态条件下都表现出在表皮中的长期持久性。然而，当活性 TGFβ 受到限制或当新的 T 细胞克隆被募集到表皮时，抗原特异性 Trm 细胞比旁观者 Trm 细胞更有效地保留。在这两种情况下，基因强制的 TGFβR 信号允许旁观者 Trm 细胞像抗原特异性 Trm 细胞一样有效地存在于表皮中。因此，