Retinoic acid and TGF-β orchestrate organ-specific programs of tissue residency
Journal Title
Immunity
Publication Type
Oct 11 epub ahead of print
Abstract
Tissue-resident memory T (T(RM)) cells are integral to tissue immunity, persisting in diverse anatomical sites where they adhere to a common transcriptional framework. How these cells integrate distinct local cues to adopt the common T(RM) cell fate remains poorly understood. Here, we show that whereas skin T(RM) cells strictly require transforming growth factor β (TGF-β) for tissue residency, those in other locations utilize the metabolite retinoic acid (RA) to drive an alternative differentiation pathway, directing a TGF-β-independent tissue residency program in the liver and synergizing with TGF-β to drive T(RM) cells in the small intestine. We found that RA was required for the long-term maintenance of intestinal T(RM) populations, in part by impeding their retrograde migration. Moreover, enhanced RA signaling modulated T(RM) cell phenotype and function, a phenomenon mirrored in mice with increased microbial diversity. Together, our findings reveal RA as a fundamental component of the host-environment interaction that directs immunosurveillance in tissues.
Keywords
CD8(+) T cells; Iel; T cell memory; TRM cells; dirty mice; mucosal immunity; retinoic acid; tissue-resident memory T cells; transforming growth factor beta
Research Division(s)
Bioinformatics
PubMed ID
39406245
Terms of Use/Rights Notice
Refer to copyright notice on published article.


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