Mucocutaneous IL-17 immunity in mice and humans: host defense vs. excessive inflammation

Mucosal Immunol. 2018 May;11(3):581-589. doi: 10.1038/mi.2017.97. Epub 2017 Nov 29.


Interleukin (IL)-17A is a pro-inflammatory cytokine in mice and humans. It is recognized as a key factor for the protection of mice against various pathogens, but it also underlies pathogenic inflammatory responses in numerous mouse models. The inborn errors of IL-17A- and IL-17F-mediated immunity identified in humans in the last decade have revealed that IL-17A and IL-17F are key players in mucocutaneous immunity to Candida albicans, and, to a lesser extent, Staphylococcus aureus. By contrast, there is currently no genetic evidence for a causal link between excess of IL-17 and autoimmunity, autoinflammation, or allergy in humans. We discuss here the physiological and pathological roles of mouse and human IL-17A and IL-17F in host defense and excessive inflammation. We highlight recent advances in our understanding of the consequences of deficient or excessive IL-17 immunity at various mucocutaneous sites, including the oral cavity, skin, intestine, lungs, and vagina.

Publication types

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

MeSH terms

  • Animals
  • Communicable Diseases / immunology*
  • Disease Models, Animal
  • Host-Pathogen Interactions
  • Humans
  • Immunity, Mucosal
  • Inflammation / immunology*
  • Interleukin-17 / genetics
  • Interleukin-17 / metabolism*
  • Mice
  • Mucous Membrane / immunology*
  • Mucous Membrane / microbiology


  • IL17A protein, human
  • IL17F protein, human
  • Il17a protein, mouse
  • Interleukin-17