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IL-4 Regulates Chemokine CCL26 in Keratinocytes through the Jak1, 2/Stat6 Signal Transduction Pathway: Implication for Atopic Dermatitis

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Title: IL-4 Regulates Chemokine CCL26 in Keratinocytes through the Jak1, 2/Stat6 Signal Transduction Pathway: Implication for Atopic Dermatitis
Author(s): Bao, Lei; Shi, Vivian Y.; Chan, Lawrence S.
Subject(s): IL-4 CCL26 Gene regulation Atopic dermatitis
Abstract: Atopic dermatitis (AD), a chronic, pruritic, inflammatory skin disease, is histopathologically characterized by epidermal hyperplasia and infiltration of T cells, mast cells, and eosinophils. Clinical study and basic research have established that IL-4 plays an important role in the pathogenesis of AD. In this report, using HaCat cells, we show that CCL26, a chemokine for eosinophils, is up-regulated by IL-4 at both the mRNA and protein levels. IL-4 also enhances CCL26 promoter activity. Serial 5’ deletion of the promoter and mutagenesis study reveal that the proximal Stat site is the key response element for IL-4 regulation of CCL26. Although IL-4 increases phosphorylation of both Stat3 and Stat6, it only activates Stat6 as shown by dominant negative studies. In addition, we found that IL-4 induces Stat6 nuclear translocation and stimulates phosphorylation of Jak1 and Jak2 but not Tyk2. IL-4 up-regulation of CCL26 can be suppressed by Jak inhibitors in a dose-dependent manner. Taken together, results of this investigation reveal that IL-4 signals through the Jak1, 2/Stat6 pathway in keratinoctyes to stimulate CCL26 expression and this may provide an explanation for the pathogenesis of AD.
Issue Date: 2012-02
Publisher: Elsevier
Citation Info: Bao, L., Shi, V. Y., & Chan, L. S. 2012. IL-4 regulates chemokine CCL26 in keratinocytes through the Jak1, 2/Stat6 signal transduction pathway: Implication for atopic dermatitis.Molecular Immunology, 50(1-2):91-97. DOI: 10.1016/j.molimm.2011.12.008
Type: Article
Description: NOTICE: this is the author’s version of a work that was accepted for publication in Molecular Immunology. Changes resulting from the publishing process, such as peer review, editing, corrections, structural formatting, and other quality control mechanisms may not be reflected in this document. Changes may have been made to this work since it was submitted for publication. A definitive version was subsequently published in Molecular Immunology, [Vol 50, Issue 1-2, Feb 2012. DOI: 10.1016/j.molimm.2011.12.008
URI: http://hdl.handle.net/10027/8528
ISSN: 0161-5890
Sponsor: Albert H. and Mary Jane Slepyan Endowed Fellowship and the University of Illinois
Date Available in INDIGO: 2012-08-17
 

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