Type I interferons (IFNs) are the first line of defence after various infections, and, as immunomodulatory 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 pathogenesis 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 vulnerable to bacterial and fungal attacks.
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Tilg et al. (2009) studied this question.
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