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Glutathione peroxidase 1 deficiency attenuates allergen-induced airway inflammation by suppressing th2 and th17 cell development

Title
Glutathione peroxidase 1 deficiency attenuates allergen-induced airway inflammation by suppressing th2 and th17 cell development
Authors
Won H.Y.Sohn J.H.Min H.J.Lee K.Woo H.A.Ho Y.-S.Park J.W.Rhee S.G.Hwang E.S.
Ewha Authors
이서구황은숙우현애
SCOPUS Author ID
이서구scopusscopus; 황은숙scopus; 우현애scopus
Issue Date
2010
Journal Title
Antioxidants and Redox Signaling
ISSN
1523-0864JCR Link
Citation
vol. 13, no. 5, pp. 575 - 587
Indexed
SCI; SCIE; SCOPUS WOS scopus
Abstract
Engagement of T cell receptor (TCR) triggers signaling pathways that mediate activation, proliferation, and differentiation of T lymphocytes. Such signaling events are mediated by reactive oxygen species (ROS), including hydrogen peroxide and lipid peroxides, both of which are reduced by glutathione peroxidase 1 (GPx1). We have now examined the role of GPx1 in the activation, differentiation, and functions of CD4+ T helper (Th) cells. TCR stimulation increased the intracellular ROS concentration in Th cells in a time-dependent manner, and such TCR-induced ROS generation was found to promote cell proliferation. GPx1-deficient Th cells produced higher levels of intracellular ROS and interleukin-2 than wild-type Th cells and proliferated at a faster rate than did wild-type cells. Moreover, differentiation of GPx1-deficient Th cells was biased toward Th1, and Th17 cell development was also impeded by GPx1 depletion. Consistent with these findings, GPx1-null mice were protected from the development of ovalbumin-induced allergic asthma. Eosinophil infiltration, goblet cell hyperplasia, collagen deposition, and airway hyperresponsiveness were thus all attenuated in the lungs of GPx1-null mice. These data indicate that GPx1-dependent control of intracellular ROS accumulation is important not only for regulation of Th cell proliferation but for modulation of differentiation into Th1, Th2, and Th17 cells. © 2010 Mary Ann Liebert, Inc.
DOI
10.1089/ars.2009.2989
Appears in Collections:
일반대학원 > 생명·약학부 > Journal papers
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