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- W2800535568 abstract "Rosacea is a common inflammatory skin disorder characterised by recurrent flare-ups. Cathelicidin antimicrobial peptides such as LL37 have been implicated in rosacea though the pathogenic mechanisms that lead to flare-ups remain elusive. In gene expression analyses, we find overexpression of type-I interferon (IFN) selectively in skin lesions of acute flare-ups but not in stabilised lesions. Using an established in vivo model of rosacea, we find pDCs largely responsible for IFN expression in situ. Moreover, the induction of the predominant TH17/22 profile, similar to the signature found in the skin of our patient cohort, is dependent on pDC-derived IFN. These findings were confirmed in transgenic mice overexpressing the protease KLK5, which is increased in rosacea and known to cleave active LL37 from its precursor protein. Furthermore, B. oleronius, a bacterium that thrives in rosacea, is exquisitely sensitive to killing by LL37 and can potently activate pDCs to produce IFN when in presence of LL37. Taken together, our data indicate that proteolytic activation of LL37, along with skin microbes linked to rosacea severity, lead to rapid pDC activation. In turn, pDC-derived IFN plays a pathogenic role in inducing a predominant TH17/22 profile thereby driving flare ups of rosacea. As TH17/22 cytokines lead to further overexpression of cathelicidins, we provide evidence for a self-sustained feedback loop amplifying inflammation in rosacea. Our study identifies a pathogenic KLK5-LL37-pDC-IFN axis in rosacea and mechanistically links B. oleronius to the induction of rosacea skin lesions." @default.
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- W2800535568 date "2018-05-01" @default.
- W2800535568 modified "2023-10-01" @default.
- W2800535568 title "931 Pathogenic role for KLK5 LL37 pDC type I interferon axis linking B. oleronius to flare ups of rosacea" @default.
- W2800535568 doi "https://doi.org/10.1016/j.jid.2018.03.943" @default.
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