IL-17 and therapeutic kynurenines in pathogenic inflammation to fungi.

摘要: 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 inflammation on infection. Some degree is required for protection, particularly in mucosal tissues, during transitional response occurring between rapid slower response. However, progressive worsens disease ultimately prevents pathogen eradication. IDO, tryptophan catabolites (“kynurenines”), regulatory help tame overzealous exaggerated inflammatory responses. In this context, IL-23 Th17 pathway, which down-regulate catabolism, may instead favor pathology serve accommodate seemingly paradoxical association chronic fungal persistence. Recent data support a view IL-23/IL-17 antagonistic strategies, including administration synthetic kynurenines, could represent new means harnessing or potentially harmful inflammation.