Interleukin-31:A new link between T cells, pruitus and atopic skin inflammation

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Pruritus is a dominant symptom of atopic skin inflammation and severely affects the quality of life of affected patients. Despite recent advances in the understanding of the immunopathogenesis of atopic skin inflammation, the underlying mechanisms of pruritus are still poorly understood. Recently, it has been shown that interleukin-31 (IL-31), a novel T cellderived cytokine, induces severe pruritus and dermatitis in transgenic mice, and signals through a heterodimeric receptor composed of interleukin-31 receptor A (IL-31RA) and oncostatin M receptor (OSMR). In a recent study, the applicants showed that IL-31 was significantly overexpressed in `pruritic’ atopic compared to ‘low- or non-pruritic’ psoriatic skin inflammation. Highest IL-31 levels were detected in prurigo nodularis, representing one of the pruritic forms of skin inflammation. In-vivo, staphylococcal superantigen rapidly induced IL-31 expression in atopic individuals. In-vitro, staphylococcal enterotoxin B but not viruses or Th1 and Th2 cytokines induced IL-31 in leukocytes. Furthermore, activated leukocytes of atopic dermatitis patients expressed IL-31 at significantly higher levels, as compared to control subjects. IL-31RA showed most abundant expression in dorsal root ganglia representing the site where the cell bodies of cutaneous sensory neurons reside. Our findings provide a new link between staphylococcal colonization, subsequent T cell recruitment/activation and pruritus induction in atopic dermatitis patients. Taken together, IL-31 may represent a novel and promising target for antipruritic drug development.