| First Author | Fowell DJ | Year | 1999 |
| Journal | Immunity | Volume | 11 |
| Issue | 4 | Pages | 399-409 |
| PubMed ID | 10549622 | Mgi Jnum | J:109489 |
| Mgi Id | MGI:3629014 | Doi | 10.1016/s1074-7613(00)80115-6 |
| Citation | Fowell DJ, et al. (1999) Impaired NFATc translocation and failure of Th2 development in Itk-deficient CD4+ T cells. Immunity 11(4):399-409 |
| abstractText | Naive 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. |
