Abstract
Psoriasis is a chronic inflammatory skin disease with disturbed interplay between immune cells and keratinocytes. Here we identify a microRNA-mediated mechanism by which IFN-γ primes keratinocytes to inflammatory stimuli. Treatment with IFN-γ results in a quick and long-lasting suppression of miR-149 in keratinocytes. Depletion of miR-149 in keratinocytes results in wide- spread transcriptomic changes and induction of inflammatory mediators with an enrichment of the TWEAK-pathway. We demonstrate that IFN-γ primes keratinocytes to TWEAK-induced IL-6 expression and this is mediated by suppression of miR-149.
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