28 May Genes That Activate Inflammation in Psoriasis Identified
MedicalResearch.com Interview with:
Ryuta Muromoto, Ph.D.
Department of Immunology,
Faculty of Pharmaceutical Sciences, Hokkaido University
MedicalResearch.com: What is the background for this study?
Dr. Muromoto: Psoriasis is an immune-mediated chronic inflammatory skin disorder that affects some 125 million people worldwide. It is characterized by itchy, scaly skin plaques. It has been known that a cytokine IL-17A, which is produced by immune cells, plays a central role in the development and maintenance of clinical features of psoriasis. IL-17A acts on keratinocytes and up-regulates anti-microbial peptides and a set of chemokines, that are important for immune cell infiltration. This immune cell feedback amplifies psoriatic inflammation. Also, other inflammatory cytokines such as TNF-alpha and interferon-gamma are up-regulated, and have been implicated in pathogenesis of psoriasis. So, the interplay between cytokines appears to be important for development of psoriasis through keratinocyte activation. In this study, we sought to clarify the actual role of IL-17A and its interplay with other cytokines in keratinocyte activation.
MedicalResearch.com: What are the main findings?
Response: We have found a simple in vitro method that can induce the expression of psoriasis-related genes in keratinocytes and so we could estimate the clinical relevance of the gene set regulated by IL-17A by comparison with previously published psoriasis transcriptome data.
MedicalResearch.com: What should readers take away from your report?
Response: We identified a set of psoriasis-related genes in keratinocytes that are regulated by IL-17A. One of these genes in particular, called NFKBIZ, was found to have a significant role in the IL-17A pathway. The comprehensive gene expression data presented in our study should be useful for furthering the understanding of the IL-17A signaling pathway in keratinocytes.
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Int Immunol. 2016 Mar 3. pii: dxw011.
IL-17A plays a central role in the expression of psoriasis signature genes through the induction of IκB-ζ in keratinocytes.
Muromoto R1, Hirao T2, Tawa K2, Hirashima K2, Kon S2, Kitai Y2, Matsuda T2.
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