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NFAT1 and JunB cooperatively regulate IL-31 gene expression in CD4+ T cells in health and disease

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Title
NFAT1 and JunB cooperatively regulate IL-31 gene expression in CD4+ T cells in health and disease
Author(s)
Ji Sun Hwang; Gi-Cheon Kim; EunBee Park; Jung-Eun Kim; Chang-Suk Chae; Won Hwang; Changhon Lee; Sung-Min Hwang; Hui Sun Wang; Jun C.-D.; Dipayan Rudra; Sin-Hyeog Im
Publication Date
2015-02
Journal
JOURNAL OF IMMUNOLOGY, v.194, no.4, pp.1963 - 1974
Publisher
AMER ASSOC IMMUNOLOGISTS
Abstract
IL-31 is a key mediator of itching in atopic dermatitis (AD) and is preferentially produced by activated CD4+ T cells and Th2 cells. Although pathophysiological functions of IL-31 have been suggested in diverse immune disorders, the molecular events underlying IL-31 gene regulation are still unclear. In this study we identified the transcription start site and functional promoter involved in IL-31 gene regulation in mouse CD4+ T cells. TCR stimulation.dependent IL-31 expression was found to be closely linked with in vivo binding of NFAT1 and JunB to the IL-31 promoter. Although NFAT1 alone enhanced IL-31 promoter activity, it was further enhanced in the presence of JunB. Conversely, knockdown of either NFAT1 or JunB resulted in reduced IL-31 expression. NFAT1-deficient CD4+ T cells showed a significant defect in IL-31 expression compared with wild-type CD4+ T cells. In agreement with these findings, mice subjected to atopic conditions showed much higher levels of IL-31, which were closely correlated with a significant increase in the number of infiltrated NFAT1+CD4+ T cells into the AD ears. Amelioration of AD progression by cyclosporin A treatment was well correlated with downregulation of IL-31 expressions in CD4+ T cells and total ear residual cells. In summary, our results suggest a functional cooperation between NFAT1 and JunB in mediating IL-31 gene expression in CD4+ T cells and indicate that interference with this interaction or their activity has the potential of reducing IL-31.mediated AD symptoms.
URI
https://pr.ibs.re.kr/handle/8788114/2123
ISSN
0022-1767
Appears in Collections:
Academy of Immunology and Microbiology(면역 미생물 공생 연구단) > Journal Papers (저널논문)
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