NDLI: Cutting edge: IL-17-secreting innate lymphoid cells are essential for host defense against fungal infection.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Wangler, Nicolette Gladiator, André Trautwein-Weidner, Kerstin LeibundGut-Landmann, Salomé
Description	Country affiliation: Switzerland Author Affiliation: Gladiator A ( Institute of Microbiology, Swiss Federal Institute of Technology Zürich, 8093 Zurich, Switzerland.)
Abstract	IL-17-mediated immunity has emerged as a crucial host defense mechanism against fungal infections. Although Th cells are generally thought to act as the major source of IL-17 in response to Candida albicans, we show that fungal control is mediated by IL-17-secreting innate lymphoid cells (ILCs) and not by Th17 cells. By using a mouse model of oropharyngeal candidiasis we found that IL-17A and IL-17F, which are both crucial for pathogen clearance, are produced promptly upon infection in an IL-23-dependent manner, and that ILCs in the oral mucosa are the main source for these cytokines. Ab-mediated depletion of ILCs in RAG1-deficient mice or ILC deficiency in retinoic acid-related orphan receptor c(-/-) mice resulted in a complete failure to control the infection. Taken together, our data uncover the cellular basis for the IL-23/IL-17 axis, which acts right at the onset of infection when it is most needed for fungal control and host protection.
ISSN	00221767
e-ISSN	15506606
Journal	The Journal of Immunology
Issue Number	2
Volume Number	190
Language	English
Publisher	The American Association of Immunologists
Publisher Date	2013-01-15
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Candida Albicans Immunology Candidiasis Immunity, Innate Th17 Cells Adaptive Immunity Animals Genetics Metabolism Candidiasis, Oral Host-pathogen Interactions Interleukin-17 Mice Mice, Knockout Research Support, Non-u.s. Gov't Discipline Immunology
Content Type	Text
Resource Type	Article
Subject	Immunology and Allergy Immunology

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