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Psoriasis: HELP
Articles by Christopher Adase
Based on 1 article published since 2010
(Why 1 article?)
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Between 2010 and 2020, Christopher Adase wrote the following article about Psoriasis.
 
+ Citations + Abstracts
1 Article Antimicrobial Peptide LL37 and MAVS Signaling Drive Interferon-β Production by Epidermal Keratinocytes during Skin Injury. 2016

Zhang, Ling-Juan / Sen, George L / Ward, Nicole L / Johnston, Andrew / Chun, Kimberly / Chen, Yifang / Adase, Christopher / Sanford, James A / Gao, Nina / Chensee, Melanie / Sato, Emi / Fritz, Yi / Baliwag, Jaymie / Williams, Michael R / Hata, Tissa / Gallo, Richard L. ·Department of Dermatology, University of California, San Diego, La Jolla, CA 92093, USA. · Department of Dermatology, University of California, San Diego, La Jolla, CA 92093, USA; Department of Cellular and Molecular Medicine, San Diego, La Jolla, CA 92093, USA. · Department of Dermatology, Case Western Reserve University, Cleveland, OH 44106, USA. · Department of Dermatology, University of Michigan, Ann Arbor, MI 48109, USA. · Department of Dermatology, University of California, San Diego, La Jolla, CA 92093, USA. Electronic address: rgallo@ucsd.edu. ·Immunity · Pubmed #27438769.

ABSTRACT: Type 1 interferons (IFNs) promote inflammation in the skin but the mechanisms responsible for inducing these cytokines are not well understood. We found that IFN-β was abundantly produced by epidermal keratinocytes (KCs) in psoriasis and during wound repair. KC IFN-β production depended on stimulation of mitochondrial antiviral-signaling protein (MAVS) by the antimicrobial peptide LL37 and double stranded-RNA released from necrotic cells. MAVS activated downstream TBK1 (TANK-Binding Kinase 1)-AKT (AKT serine/threonine kinase 1)-IRF3 (interferon regulatory factor 3) signaling cascade leading to IFN-β production and then promoted maturation of dendritic cells. In mice, the production of epidermal IFN-β by LL37 required MAVS, and human wounded and/or psoriatic skin showed activation of MAVS-associated IRF3 and induction of MAVS and IFN-β gene signatures. These findings show that KCs are an important source of IFN-β and MAVS is critical to this function, and demonstrates how the epidermis triggers unwanted skin inflammation under disease conditions.