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• W2028842451 abstract "Naive Itk-deficient CD4+ T cells were unable to establish stable IL-4 production, even when primed in Th2-inducing conditions. In contrast, IFNγ 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 IFNγ expression." @default.
• W2028842451 created "2016-06-24" @default.
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• W2028842451 date "1999-10-01" @default.
• W2028842451 modified "2023-10-17" @default.
• W2028842451 title "Impaired NFATc Translocation and Failure of Th2 Development in Itk-Deficient CD4+ T Cells" @default.
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• W2028842451 doi "https://doi.org/10.1016/s1074-7613(00)80115-6" @default.
• W2028842451 hasPubMedId "https://pubmed.ncbi.nlm.nih.gov/10549622" @default.
• W2028842451 hasPublicationYear "1999" @default.
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