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- W1524549627 abstract "Abstract CD4+ T cells with a block in the NF-κB signaling pathway exhibit decreases in Th1 responses and diminished nuclear levels of multiple transactivating NF-κB/Rel/IκB proteins. To determine the lineage-intrinsic contributions of these transactivators to Th differentiation, T cells from mice deficient in specific subunits were cultured in exogenous cytokines promoting either Th1 or Th2 differentiation. RelB-deficient cells exhibited dramatic defects in Th1 differentiation and IFN-γ production, whereas no consistent defect in either Th1 or Th2 responses was observed with c-Rel-deficient cells. In sharp contrast, Bcl-3-null T cells displayed no defect in IFN-γ production, but their Th2 differentiation and IL-4, IL-5, and IL-13 production were significantly impaired. The absence of RelB led to a dramatic decrease in the expression of T-box expressed in T cells and Stat4. In contrast, Bcl-3-deficient cells exhibited decreased GATA-3, consistent with evidence that Bcl-3 can transactivate a gata3 promoter. These data indicate that Bcl-3 and RelB exert distinct and opposing effects on the expression of subset-determining transcription factors, suggesting that the characteristics of Th cell responses may be regulated by titrating the stoichiometry of transactivating NF-κB/Rel/IκB complexes in the nuclei of developing helper effector cells." @default.
- W1524549627 created "2016-06-24" @default.
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- W1524549627 date "2005-08-15" @default.
- W1524549627 modified "2023-10-16" @default.
- W1524549627 title "Opposing Roles for RelB and Bcl-3 in Regulation of T-Box Expressed in T Cells, GATA-3, and Th Effector Differentiation" @default.
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- W1524549627 doi "https://doi.org/10.4049/jimmunol.175.4.2102" @default.
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