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.
This article is featured in In This Issue, p.555
N.Z. is supported by National Institutes of Health Grant R01-AI125701, the Young Investigator Award from the Max and Minnie Tomerlin Voelcker Fund, the University of Texas Rising Star Award, and a pilot grant from the School of Medicine at The University of Texas Health Science Center at San Antonio.
The online version of this article contains supplemental material.
Abbreviations used in this article:
- lymphocytic choriomeningitis virus
- P-selectin glycoprotein ligand-1
- tissue-resident memory T.
- Received August 30, 2016.
- Accepted November 8, 2016.
- Copyright © 2017 by The American Association of Immunologists, Inc.