TGF-β Controls the Formation of Kidney-Resident T Cells via Promoting Effector T Cell Extravasation

Tissue-resident memory T (T-RM) cells, a population of noncirculating memory T cells, are one of the essential components of immunological memory in both mouse and human. Although CD69(+) CD103(+) T-RM cells represent a major T-RM cell population in barrier tissues including the mucosal surface and the skin, CD69(+) CD103(-) T-RM cells dominate most nonbarrier tissues, such as the kidney. TGF-beta is required for the differentiation of CD69(+) CD103(+) T-RM cells in barrier tissues. However, the developmental control of CD69(+) CD103(-) T-RM cells in nonbarrier tissues remains largely unknown and the involvement of TGF-beta signaling is less clear. In this study we demonstrated that TGF-beta promoted the formation of kidney-resident T cells via enhancing the tissue entry of effector T cells. Mechanistically, TGF-beta enhanced E-and P-selectin and inflammatory chemokine-mediated extravasation of effector T cells. Thus TGF-beta controls the first developmental checkpoint of TRM cell differentiation in nonbarrier tissues.