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Dysregulated skin barrier function in Tmem79 mutant mice promotes IL-17A-dependent spontaneous skin and lung inflammation.

Sean P SaundersAchilleas FloudasTara MoranCiara M ByrneMichael D RooneyCaoimhe M R FahyJoan A GeogheganYoichiro IwakuraPadraic G FallonChristian Schwartz
Published in: Allergy (2020)
Mice lacking Tmem79/Mattrin expression have a defective skin barrier. In adulthood, these mice develop dermatitis with secondary progression to lung inflammation. The development of skin and lung inflammation is IL-17A-dependent and mediated by TCRγδ T cells.
Keyphrases
  • oxidative stress
  • soft tissue
  • wound healing
  • high fat diet induced
  • wild type
  • type diabetes
  • metabolic syndrome
  • regulatory t cells
  • dendritic cells
  • early life