Abstract
Effective alopecia areata (AA) therapy requires targeting of the underlying key pathomechanisms, namely hair follicle (HF) immune privilege (IP) collapse and premature catagen. Based on mouse data, the multi-functional, anti-apoptotic, autoimmunity-promoting cytokine, interleukin-15 (IL-15), is often postulated to be a key pathogenic cytokine in human AA, even though it is unclear how IL-15 affects HF-IP and catagen. Here, we show that lesional skin of AA patients shows an increased number of perifollicular IL-15+ T and NK cells.
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