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Exogenous Hydrogen Peroxide Induces Lipid Raft-Mediated STAT-6 Activation in T Cells

Title
Exogenous Hydrogen Peroxide Induces Lipid Raft-Mediated STAT-6 Activation in T Cells
Authors
Kim H.J.Lim J.Jang Y.-S.Shin E.-C.Kim H.-R.Seoh J.-Y.Lee J.S.Lee S.N.Kang J.L.Choi Y.-H.
Ewha Authors
서주영이순남최윤희
SCOPUS Author ID
서주영scopus; 이순남scopus; 최윤희scopus
Issue Date
2017
Journal Title
Cellular Physiology and Biochemistry
ISSN
1015-8987JCR Link
Citation
vol. 42, no. 6, pp. 2467 - 2480
Keywords
IL-4Lipid raftsReactive oxygen species (ROS)STAT-6Th2 cells
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Background/Aims: CD4+ T cells are a critical component of the adaptive immune response. While the mechanisms controlling the differentiation of the Th1, Th17, and regulatory T cell subsets from naïve CD4+ T cells are well described, the factors that induce Th2 differentiation are still largely unknown. Methods: The effects of treatment with exogenous H2O2 on STAT-6 phosphorylation and activation in T cells were examined by immunoblotting, immunofluorescence and gel shift assay. Anti-CD3 antibody and methyl-β-cyclodextrin were utilized to induce lipid raft assembly and to investigate the involvement of lipid rafts, respectively. Results: Jurkat and EL-4 T cells that were exposed to H2O2 showed rapid and strong STAT-6 phosphorylation, and the extent of STAT-6 phosphorylation was enhanced by co-treatment with anti-CD3 antibody. The effect of H2O2 on STAT-6 phosphorylation and translocation was inhibited by disruption of lipid rafts. STAT-6 activation in response to H2O2 treatment regulated IL-4 gene expression, and this response was strengthened by treatment with anti-CD3. Conclusion: Our results indicate that reactive oxygen species such as H2O2 can act on upstream and initiating factors for activation of STAT-6 in T cells and contribute to formation of a positive feedback loop between STAT-6 and IL-4 in the Th2 differentiation process. © 2017 Published by S. Karger AG, Basel.
DOI
10.1159/000480210
Appears in Collections:
의학전문대학원 > 의학과 > Journal papers
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