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Chemokine receptors in the pathogenesis and therapy of psoriasis

Published:December 16, 2011DOI:https://doi.org/10.1016/j.jdermsci.2011.11.007

      Abstract

      Chemokine receptors are G-protein-coupled, seven-transmembrane-spanning surface receptors that play key roles in cell trafficking, cell motility, and survival. These receptors are activated by small molecular weight chemotactic cytokines called chemokines. Chemokine receptors and their corresponding chemokine ligands play roles in the migration and localization of normal T cells (and other cells) during physiological responses in inflamed or infected skin. In psoriasis, the chemokine receptor CCR6 is expressed on the Th17 cells and γδ T cells, which produce a variety of cytokines (IL17 and IL22 among others), that play a role in the immunological activation. CCR6 and its ligand, CCL20, are highly expressed in psoriatic skin lesion and CCR6 is essential for the development of the psoriasiform phenotype following IL23 injection in mouse skin. In this review, we focus on the roles of chemokine receptors, particularly of CCR6, in the pathogenesis of psoriasis and discuss chemokine receptors as novel therapeutic targets for psoriasis.

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      Biography

      Tomotaka Mabuchi, is an assistant professor in Department of Dermatology, Tokai University School of Medicine, Kanagawa, Japan (Chief: Prof. Akira Ozawa). He graduated from Tokai University school of Medicine in 1999. He has performed research on the genetics of psoriasis in the Department of Molecular Life Science, Tokai University School of Medicine (Chief: Prof. Hidetoshi Inoko) and received his Ph.D. degree from Tokai University in 2007. He was secretary general of the 24th Annual Meeting of the Japanese Society for Psoriasis Research in 2009. Since 2009, he has conducted research on the immunology of psoriasis in the Department of Dermatology, Medical College of Wisconsin, WI, USA (PI: Prof. Sam T. Hwang).