DEAR EDITOR, Psoriasis is a frequent, chronic recurrent inflammatory skin disease that substantially affects patients’ quality of life. Interleukin (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 psoriasis. 1 However, the cellular sources of IL-17A in psoriasis are still debated. T helper (Th) 17 cells have been suggested as major contributors, 2, 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 so-called Munro’s microabscesses–stain strongly positive for IL-17A, while in the dermal compartment IL-17A is found mainly in mast cells, less so in neutrophils and only rarely in T cells. 3–5

The role of mast cells as a possible source of IL-17A in vivo remains debated. IL-17A transcripts were found in mast cells cultured upon dissection of psoriatic skin6 and CD34-derived mast cells were shown to produce IL-17A in a RORC-dependent manner in vitro. 7 However, tonsil-derived mast cells and LAD2 mast cell lines were reported to lack IL-17A transcription machinery and rather to capture exogenous IL-17A in vitro. 8, 9 The discrepancy between these studies might reflect the use of mast cells derived from different tissues or technical artefacts introduced by the