TGF-β Controls the Formation of Kidney-Resident T Cells via Promoting Effector T Cell Extravasation
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Updated: Mar 11, 2026

Isolation of Double Negative αβ T Cells from the Kidney
Published on: May 16, 2014
Chaoyu Ma1, Shruti Mishra1, Erika L Demel1
1Department of Microbiology, Immunology and Molecular Genetics, School of Medicine, University of Texas Health San Antonio, San Antonio, TX 78229.
Abstract:
Tissue-resident memory T (TRM) 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+ TRM cells represent a major TRM cell population in barrier tissues including the mucosal surface and the skin, CD69+CD103- TRM cells dominate most nonbarrier tissues, such as the kidney. TGF-β is required for the differentiation of CD69+CD103+ TRM cells in barrier tissues. However, the developmental control of CD69+CD103- TRM 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 TRM cell differentiation in nonbarrier tissues.
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