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

Research output: Contribution to journalArticle

  • External authors:
  • Nicolas Dutzan
  • Loreto Abusleme
  • Hayley Bridgeman
  • Teresa Greenwell-Wild
  • Tamsin Zangerle Murray
  • Mark Fife
  • Nicolas Bouladoux
  • Holly Linley
  • Laurie Brenchley
  • Kelly Wemyss
  • Gloria Calderon
  • Bo-Young Hong
  • Timothy. J Break
  • Dawn. M. E Bowdish
  • Michail. S Lionakis
  • Simon A Jones
  • Giorgio Trinchieri
  • Patricia.I. Diaz
  • Yasmine Belkaid
  • Niki M Moutsopoulos

Abstract

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.

Bibliographical metadata

Original languageEnglish
JournalImmunity
Early online date10 Jan 2017
DOIs
StatePublished - 17 Jan 2017