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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.

Author information

1
St. Giles Laboratory of Human Genetics of Infectious Diseases, Rockefeller Branch, The Rockefeller University, New York, NY, USA.
2
Laboratory of Human Genetics of Infectious Diseases, Necker Branch, INSERM U1163, Paris, France.
3
Paris Descartes University, Imagine Institute, Paris, France.
4
Pediatric Hematology-Immunology Unit, Necker Hospital for Sick Children, Paris, France.
5
Howard Hughes Medical Institute, New York, NY, USA.

Abstract

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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