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

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

Li J1, Casanova JL1,2,3,4,5, Puel A1,2,3.

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St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY, USA.
Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Paris, France.
Paris Descartes University, Imagine Institute, Paris, France.
Pediatric Hematology-Immunology Unit, Necker Hospital for Sick Children, Paris, France.
Howard Hughes Medical Institute, New York, NY, USA.


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.

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