Desired response to phototherapy vs photoaggravation in psoriasis: what makes the difference?. Issue 12 (29th November 2016)

• Record Type: Journal Article
• Authors: Wolf, Peter; Weger, Wolfgang; Patra, VijayKumar; Gruber‐Wackernagel, Alexandra; Byrne, Scott N.
• Other Names: Wolf Peter guestEditor.; de Gruijl Frank guestEditor.
• Is Part Of: Experimental dermatology. Volume 25:Issue 12(2016)
• Page Start: 937
• Page End: 944
• Publication Date: 2016-11-29
• Subjects: Koebner phenomenon -- photoaggravation -- photosensitivity -- phototherapy -- polymorphic light eruption -- psoriasis; Dermatology -- Periodicals; 616.5
• DOI: 10.1111/exd.13137
• Languages: English
• ISSNs: 0906-6705

Abstract

Abstract: Psoriasis commonly responds beneficially to UV radiation from natural sunlight or artificial sources. Therapeutic mechanisms include the proapoptotic and immunomodulating effects of UV, affecting many cells and involving a variety of pro‐ and anti‐inflammatory cytokines, downregulating the Th17/IL‐23 response with simultaneous induction of regulatory immune cells. However, exposure to UV radiation in a subset of psoriasis patients leads to exacerbation of the disease. We herein shed light on the predisposing factors of photosensitive psoriasis, including genetics (such as HLA‐Cw*0602 or CARD14), gender and coexisting photodermatoses such as polymorphic light eruption (PLE) in the context of potential molecular mechanisms behind therapeutic photoresponsiveness or photoaggravation. UV‐induced damage/pathogen‐associated molecular patterns, damage to self‐coding RNA (signalling through Toll‐like receptors), certain antimicrobial peptides and/or inflammasome activation may induce innate immunity, leading to psoriasis at the site of UV exposure when there is concomitant, predisposing resistance against UV‐induced suppression of the adaptive immune response (like in PLE) that otherwise would act to reduce psoriasis.