Open Access

REVIEW

Suppression of interleukin-17 by type I interferons: a contributing factor in virus-induced immunosuppression?

Herbert Tilg, Alexander R. Moschen, Arthur Kaser

Christian Doppler Research Laboratory for Gut Inflammation and Department of Gastroenterology and Hepatology, Medical University Innsbruck, Anichstrasse 35, 6020 Innsbruck, Austria

* Corresponding Author: H. Tilg,

European Cytokine Network 2009, 20(1), 1-6. https://doi.org/10.1684/ecn.2009.0141

Accepted 23 January 2009;

Abstract

Type I interferons (IFNs) are the first line of defence after various infections, and, as immuno-modulatory cytokines, bridge innate and adaptive immunity. IL-17, mainly secreted by specific T cells, has recently been identified regulating neutrophil-mediated inflammation, and has been implicated in the pathogen-esis of many acute and chronic inflammatory disorders. This cytokine is considered of critical importance for an effective anti-bacterial and anti-fungal immune response as needed subsequent to many viral infections. Recent studies have demonstrated that type I IFNs potently suppress IL-17 expression and Th17 differentiation in vitro and in vivo. Therefore, suppression of IL-17, as well as many other well-defined interactions of type I IFNs with the cytokine cascade, may contribute to virus-induced immunosuppression making the host vulnera-ble to bacterial and fungal attacks.

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Keywords

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