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pubmed-article:10549622pubmed:abstractTextNaive Itk-deficient CD4+ T cells were unable to establish stable IL-4 production, even when primed in Th2-inducing conditions. In contrast, IFNgamma production was little affected. Failure to express IL-4 occurred even among cells that had gone through multiple cell divisions and was associated with a delay in the kinetics and magnitude of NFATc nuclear localization. IL-4 production was restored genetically by retroviral reconstitution of Itk or biochemically by augmenting the calcium flux with ionomycin. In vivo, Itk-deficient mice were unable to establish functional Th2 cells. Development of protective Th1 cells was unimpeded. These data define a nonredundant role for Itk in modulating signals from the TCR/CD28 pathways that are specific for the establishment of stable IL-4 but not IFNgamma expression.lld:pubmed
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pubmed-article:10549622pubmed:articleTitleImpaired NFATc translocation and failure of Th2 development in Itk-deficient CD4+ T cells.lld:pubmed
pubmed-article:10549622pubmed:affiliationDepartment of Medicine, University of California San Francisco 94143, USA.lld:pubmed
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