BioAcyl Corp |
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| Resource type: Journal Article DOI: 10.1073/pnas.1802320115 ID no. (ISBN etc.): 0027-8424 BibTeX citation key: Krishnan2018 View all bibliographic details |
Categories: BioAcyl Corp, BioAcyl Corp Subcategories: Inmunidad de mucosas, Perodontitis Creators: Barbera, Bowdish, Bridgeman, Grainger, Konkel, Krishnan, Mahmood, McClure, O'Boyle, Prise, Schenck, Wemyss, Zaiss, Zangerle-Murray Collection: Proc. Natl. Acad. Sci. U.S.A. |
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| Abstract |
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T cells are enriched at barrier sites such as the gut, skin, and lung, where their roles in maintaining barrier integrity are well established. However, how these cells contribute to homeostasis at the gingiva, a key oral barrier and site of the common chronic inflammatory disease periodontitis, has not been explored. Here we demonstrate that the gingiva is policed by {$gamma$}{$delta$} T cells with a T cell receptor (TCR) repertoire that diversifies during development. Gingival {$gamma$}{$delta$} T cells accumulated rapidly after birth in response to barrier damage, and strikingly, their absence resulted in enhanced pathology in murine models of the oral inflammatory disease periodontitis. Alterations in bacterial communities could not account for the increased disease severity seen in {$gamma$}{$delta$} T cell-deficient mice. Instead, gingival {$gamma$}{$delta$} T cells produced the wound healing associated cytokine amphiregulin, administration of which rescued the elevated oral pathology of tcr{$delta$}{-}/{-} mice. Collectively, our results identify {$gamma$}{$delta$} T cells as critical constituents of the immuno-surveillance network that safeguard gingival tissue homeostasis
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