Opposing roles for RelB and Bcl-3 in regulation of T-box expressed in T cells, GATA-3, and Th effector differentiation

J Immunol. 2005 Aug 15;175(4):2102-10. doi: 10.4049/jimmunol.175.4.2102.

Abstract

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

Publication types

  • Research Support, N.I.H., Extramural
  • Research Support, Non-U.S. Gov't
  • Research Support, U.S. Gov't, Non-P.H.S.
  • Research Support, U.S. Gov't, P.H.S.

MeSH terms

  • Animals
  • B-Cell Lymphoma 3 Protein
  • Cell Differentiation / immunology*
  • Cells, Cultured
  • DNA-Binding Proteins / physiology
  • GATA3 Transcription Factor / biosynthesis
  • GATA3 Transcription Factor / deficiency
  • GATA3 Transcription Factor / metabolism*
  • Humans
  • Interferon-gamma / antagonists & inhibitors
  • Interferon-gamma / biosynthesis
  • Jurkat Cells
  • Mice
  • Mice, Inbred C57BL
  • Mice, Knockout
  • Mice, Transgenic
  • Polycomb Repressive Complex 1
  • Proto-Oncogene Proteins / deficiency
  • Proto-Oncogene Proteins / genetics
  • Proto-Oncogene Proteins / physiology*
  • Proto-Oncogene Proteins c-rel / biosynthesis
  • Proto-Oncogene Proteins c-rel / deficiency
  • Proto-Oncogene Proteins c-rel / metabolism
  • T-Box Domain Proteins
  • T-Lymphocytes, Helper-Inducer / cytology
  • T-Lymphocytes, Helper-Inducer / immunology*
  • Th1 Cells / cytology
  • Th1 Cells / metabolism*
  • Th2 Cells / metabolism*
  • Transcription Factors / biosynthesis
  • Transcription Factors / metabolism*

Substances

  • B-Cell Lymphoma 3 Protein
  • BCL3 protein, human
  • Bcl3 protein, mouse
  • DNA-Binding Proteins
  • GATA3 Transcription Factor
  • Gata3 protein, mouse
  • Pcgf6 protein, mouse
  • Proto-Oncogene Proteins
  • Proto-Oncogene Proteins c-rel
  • T-Box Domain Proteins
  • T-box transcription factor TBX21
  • Transcription Factors
  • Interferon-gamma
  • Polycomb Repressive Complex 1