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Department of Experimental Medicine, University of Perugia, Perugia, Italy
Largely viewed as proinflammatory, innate responses combine with adaptive immunity to generate the most effective form of antifungal resistance, and T cells exercise feedback control over diverse effects of inflammation on infection. Some degree of inflammation is required for protection, particularly in mucosal tissues, during the transitional response occurring between the rapid innate and slower adaptive response. However, progressive inflammation worsens disease and ultimately prevents pathogen eradication. IDO, tryptophan catabolites ("kynurenines"), and regulatory T cells help to tame overzealous and exaggerated inflammatory responses. In this context, IL-23 and the Th17 pathway, which down-regulate tryptophan catabolism, may instead favor pathology and serve to accommodate the seemingly paradoxical association of chronic inflammation with fungal persistence. Recent data support a view in which IL-23/IL-17 antagonistic strategies, including the administration of synthetic kynurenines, could represent a new means of harnessing progressive or potentially harmful inflammation.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 The original studies conducted in our laboratory were supported by the European Commission’s Specific Targeted Research Projects "EURAPS" (ILSHM-CT-2005) (to L.R.) and "MANASP" (LSHE-CT-2006) (to L.R.) and by funding from the Juvenile Diabetes Research Foundation (to P.P.).
2 Address correspondence and reprint requests to Dr. Luigina Romani and Dr. Paolo Puccetti, Department of Experimental Medicine and Biochemical Sciences, University of Perugia, Via del Giochetto, 06126 Perugia, Italy. E-mail addresses: lromani{at}unipg.it and plopcc{at}tin.it
3 Abbreviations used in this paper: Treg, regulatory T cell; CGD, chronic granulomatous disease; CMC, chronic mucocutaneous candidiasis; DC, dendritic cell; IRS, immune reconstitution syndrome; PMN, polymorphonuclear neutrophil; ROR, retinoic acid receptor-related orphan receptor.
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