Full metadata record
DC Field | Value | Language |
---|---|---|
dc.contributor.author | 이서구 | * |
dc.contributor.author | 황은숙 | * |
dc.contributor.author | 우현애 | * |
dc.date.accessioned | 2016-08-28T12:08:26Z | - |
dc.date.available | 2016-08-28T12:08:26Z | - |
dc.date.issued | 2010 | * |
dc.identifier.issn | 1523-0864 | * |
dc.identifier.other | OAK-6709 | * |
dc.identifier.uri | https://dspace.ewha.ac.kr/handle/2015.oak/220899 | - |
dc.description.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. | * |
dc.language | English | * |
dc.title | Glutathione peroxidase 1 deficiency attenuates allergen-induced airway inflammation by suppressing th2 and th17 cell development | * |
dc.type | Article | * |
dc.relation.issue | 5 | * |
dc.relation.volume | 13 | * |
dc.relation.index | SCI | * |
dc.relation.index | SCIE | * |
dc.relation.index | SCOPUS | * |
dc.relation.startpage | 575 | * |
dc.relation.lastpage | 587 | * |
dc.relation.journaltitle | Antioxidants and Redox Signaling | * |
dc.identifier.doi | 10.1089/ars.2009.2989 | * |
dc.identifier.wosid | WOS:000279641700002 | * |
dc.identifier.scopusid | 2-s2.0-77954895882 | * |
dc.author.google | Won H.Y. | * |
dc.author.google | Sohn J.H. | * |
dc.author.google | Min H.J. | * |
dc.author.google | Lee K. | * |
dc.author.google | Woo H.A. | * |
dc.author.google | Ho Y.-S. | * |
dc.author.google | Park J.W. | * |
dc.author.google | Rhee S.G. | * |
dc.author.google | Hwang E.S. | * |
dc.contributor.scopusid | 이서구(7401852092) | * |
dc.contributor.scopusid | 황은숙(8688011100) | * |
dc.contributor.scopusid | 우현애(8068619500) | * |
dc.date.modifydate | 20240215164922 | * |