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TGF-β Controls the Formation of Kidney-Resident T Cells via Promoting Effector T Cell Extravasation
Author(s) -
Chaoyu Ma,
Shruti Mishra,
Erika L. Demel,
Yong Liu,
Nu Zhang
Publication year - 2016
Publication title -
the journal of immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.737
H-Index - 372
eISSN - 1550-6606
pISSN - 0022-1767
DOI - 10.4049/jimmunol.1601500
Subject(s) - extravasation , microbiology and biotechnology , effector , cytotoxic t cell , cd69 , t cell , chemokine , population , immunology , biology , il 2 receptor , chemistry , inflammation , immune system , medicine , biochemistry , environmental health , in vitro
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-β 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-β signaling is less clear. In this study we demonstrated that TGF-β promoted the formation of kidney-resident T cells via enhancing the tissue entry of effector T cells. Mechanistically, TGF-β enhanced E- and P-selectin and inflammatory chemokine-mediated extravasation of effector T cells. Thus TGF-β controls the first developmental checkpoint of T RM cell differentiation in nonbarrier tissues.

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