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On-going mechanical damage from mastication drives homeostatic Th17 cell responses at the oral barrier

Dutzan, Nicolas, Abusleme, Loreto, Bridgeman, Hayley, Greenwell-Wild, Teresa, Zangerle-Murray, Tamsin, Fife, Mark E., Bouladoux, Nicolas, Linley, Holly, Brenchley, Laura, Wemys, Kelly, Calderon, Gloria, Hong, Bo-Young, Break, Timothy J., Bowdish, Dawn M. E., Lionakis, Michail S., Jones, Simon A., Trinchieri, Giorgio, Diaz, Patricia I., Belkaid, Yasmine and Konkel, Joanne E. 2017. On-going mechanical damage from mastication drives homeostatic Th17 cell responses at the oral barrier. Immunity 46 (1) , pp. 133-147. 10.1016/j.immuni.2016.12.010

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Immuno-surveillance networks operating at barrier sites are tuned by local tissue cues to ensure effective immunity. Site-specific commensal bacteria provide key signals ensuring host defense in the skin and gut. However, how the oral microbiome and tissue-specific signals balance immunity and regulation at the gingiva, a key oral barrier, remains minimally explored. In contrast to the skin and gut, we demonstrate that gingiva-resident T helper 17 (Th17) cells developed via a commensal colonization- independent mechanism. Accumulation of Th17 cells at the gingiva was driven in response to the physiological barrier damage that occurs during mastication. Physiological mechanical damage, via induction of interleukin 6 (IL-6) from epithelial cells, tailored effector T cell function, promoting increases in gingival Th17 cell numbers. These data highlight that diverse tissue-specific mechanisms govern education of Th17 cell responses and demonstrate that mechanical damage helps define the immune tone of this important oral barrier.

Item Type: Article
Date Type: Publication
Status: Published
Schools: Medicine
Systems Immunity Research Institute (SIURI)
Subjects: R Medicine > R Medicine (General)
Uncontrolled Keywords: mucosal immunology; Th17 cells; IL-17; oral immunity; barrier immunity; periodontitis; T cells
Additional Information: This is an open access article under the terms of the CC-BY license.
Publisher: Elsevier (Cell Press)
ISSN: 1074-7613
Related URLs:
Date of First Compliant Deposit: 23 January 2017
Date of Acceptance: 27 October 2016
Last Modified: 20 Jan 2021 09:30

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