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Opposing Roles for RelB and Bcl-3 in Regulation of T-Box Expressed in T Cells, GATA-3, and Th Effector Differentiation ¹

Radiah A. Corn^2,*, Chris Hunter, Hsiou-Chi Liou, Ulrich Siebenlist and Mark R. Boothby^3,¶

^* Department of Microbiology, Meharry Medical College, Nashville, TN 37208; Department of Pathobiology, School of Veterinary Medicine, University of Pennsylvania, Philadelphia, PA 19104; Department of Medicine, Division of Immunology, Cornell University Medical College, New York, NY 10021; Laboratory of Immunoregulation, National Institute of Arthritis and Infectious Diseases, National Institutes of Health, Bethesda, MD; and ^¶ Department of Microbiology and Immunology, Vanderbilt University Medical School, Nashville, TN 37232

CD4⁺ T cells with a block in the NF-B signaling pathway exhibit decreases in Th1 responses and diminished nuclear levels of multiple transactivating NF-B/Rel/IB 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- 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- 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-B/Rel/IB complexes in the nuclei of developing helper effector cells.

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