Psoriasis is a frequent, chronic recurrent inflammatory skin disease that substantially affects the quality of life of patients. IL-17A is believed to play a major role in its pathogenesis, as strategies to block this cytokine proved to be particularly effective in the treatment of psoriasis1. However, the cellular sources of IL-17A in psoriasis are still debated. Th17 cells have been suggested as major contributors2,3, although this hypothesis has been recently challenged by the histological analysis of lesional psoriatic skin from several independent groups. In the epidermis, neutrophils – forming the so-called Munro's microabscesses – stain strongly positive for IL-17A, while in the dermal compartment IL-17A is mainly found in mast cells, less so in neutrophils and only rarely in T cells3-5.
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