IL-17C regulates the innate immune function of epithelial cells in an autocrine manner

Nat Immunol. 2011 Oct 12;12(12):1159-66. doi: 10.1038/ni.2156.

Vladimir Ramirez-Carrozzi ¹, Arivazhagan Sambandam, Elizabeth Luis, Zhongua Lin, Surinder Jeet, Justin Lesch, Jason Hackney, Janice Kim, Meijuan Zhou, Joyce Lai, Zora Modrusan, Tao Sai, Wyne Lee, Min Xu, Patrick Caplazi, Lauri Diehl, Jason de Voss, Mercedesz Balazs, Lino Gonzalez Jr, Harinder Singh, Wenjun Ouyang, Rajita Pappu

Affiliations

Affiliation

1 Department of Immunology, Genentech, South San Francisco, California, USA.

PMID: 21993848 DOI: 10.1038/ni.2156

Abstract

Interleukin 17C (IL-17C) is a member of the IL-17 family that is selectively induced in epithelia by Bacterial challenge and inflammatory stimuli. Here we show that IL-17C functioned in a unique autocrine manner, binding to a receptor complex consisting of the receptors IL-17RA and IL-17RE, which was preferentially expressed on tissue epithelial cells. IL-17C stimulated epithelial inflammatory responses, including the expression of proinflammatory cytokines, chemokines and antimicrobial Peptides, which were similar to those induced by IL-17A and IL-17F. However, IL-17C was produced by distinct cellular sources, such as epithelial cells, in contrast to IL-17A, which was produced mainly by leukocytes, especially those of the T(H)17 subset of helper T cells. Whereas IL-17C promoted inflammation in an imiquimod-induced skin-inflammation model, it exerted protective functions in dextran sodium sulfate-induced colitis. Thus, IL-17C is an essential autocrine cytokine that regulates innate epithelial immune responses.

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