Narrow-band UVB radiation (NB-UVB) therapy offers a well-established treatment modality for psoriasis. However, despite the common use of this form of treatment, the mechanism of action of NB-UVB is not well understood. We studied a group of 14 patients with moderate-to-severe psoriasis treated with carefully titrated and monitored NB-UVB for 6 weeks. Lesional plaques were classified as normalized (n=8) or nonresponsive (n=6) based on their histological improvement and normalization. We characterized lesional myeloid dendritic cells (DCs) and T cells and their inflammatory mediators using immunohistochemistry and real-time PCR. NB-UVB suppressed multiple parameters of the IL-23/IL-17 pathway in normalized plaques, but not in nonresponsive plaques. NB-UVB decreased the numbers of CD11c(+) DCs, specifically CD1c(-)CD11c(+) "inflammatory" DCs, and their products, IL-20, inducible nitric oxide synthase, IL-12/23p40, and IL-23p19. Furthermore, effective NB-UVB suppressed IL-17 and IL-22 mRNAs, which strongly correlated with lesion resolution. Therefore, in addition to its known role in suppressing IFN-γ production, NB-UVB radiation therapy can also target the IL-17 pathway to resolve psoriatic inflammation.JID JOURNAL CLUB ARTICLE: For questions, answers, and open discussion about this article, please go to http://www.nature.com/jid/journalclub.
Trial registration: ClinicalTrials.gov NCT00220025.