Keratinocyte-intrinsic MHCII expression controls microbiota-induced Th1 cell responses

Proc Natl Acad Sci U S A. 2019 Nov 19;116(47):23643-23652. doi: 10.1073/pnas.1912432116. Epub 2019 Oct 31.

Abstract

The cross-talk between the microbiota and the immune system plays a fundamental role in the control of host physiology. However, the tissue-specific factors controlling this dialogue remain poorly understood. Here we demonstrate that T cell responses to commensal colonization are associated with the development of organized cellular clusters within the skin epithelium. These organized lymphocyte clusters are surrounded by keratinocytes expressing a discrete program associated with antigen presentation and antimicrobial defense. Notably, IL-22-mediated keratinocyte-intrinsic MHC class II expression was required for the selective accumulation of commensal-induced IFN-γ, but not IL-17A-producing CD4+ T cells within the skin. Taking these data together, this work uncovers an unexpected role for MHC class II expression by keratinocytes in the control of homeostatic type 1 responses to the microbiota. Our findings have important implications for the understanding of the tissue-specific rules governing the dialogue between a host and its microbiota.

Keywords: Th1; antigen presentation; keratinocyte; microbiota; skin.

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, N.I.H., Intramural
  • Research Support, Non-U.S. Gov't

MeSH terms

  • Animals
  • Antigen Presentation
  • Candida albicans / immunology
  • Epidermis / immunology
  • Epidermis / microbiology*
  • Genes, MHC Class II
  • Histocompatibility Antigens Class II / biosynthesis*
  • Host Microbial Interactions / immunology*
  • Interferon-gamma / biosynthesis
  • Keratinocytes / immunology*
  • Keratinocytes / metabolism
  • Mice
  • Mice, Inbred C57BL
  • Microbiota / immunology*
  • Organ Specificity
  • Radiation Chimera
  • Specific Pathogen-Free Organisms
  • Staphylococcus aureus / immunology
  • Staphylococcus epidermidis / immunology
  • Symbiosis
  • Th1 Cells / immunology*
  • Th1 Cells / metabolism

Substances

  • Histocompatibility Antigens Class II
  • Interferon-gamma