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Critical roles for the Bcl-3 oncoprotein in T cell-mediated immunity, splenic microarchitecture, and germinal center reactions.

Chromosomal translocations of bcl-3 are associated with chronic B cell lymphocytic leukemias. Previously, we have shown that Bcl-3, a distinct member of the I kappa B family, may function as a positive regulator of NF-kappa B activity, although its physiologic roles remained unknown. To uncover these roles, we generated Bcl-3-deficient mice. Mutant mice, but not their littermate controls, succumb to T. gondii owing to failure to mount a protective T helper 1 immune response. Bcl-3-deficient mice are also impaired in germinal center reactions and T-dependent antibody responses to influenza virus. The results reveal critical roles for Bcl-3 in antigen-specific priming of T and B cells. Altered microarchitecture of secondary lymphoid organs in mutant mice, including partial loss of B cells, may underlie the immunologic defects. The implied role of Bcl-3 in maintaining B cells in wild-type mice may related to its oncogenic potential.

Pubmed ID: 9133427

Authors

  • Franzoso G
  • Carlson L
  • Scharton-Kersten T
  • Shores EW
  • Epstein S
  • Grinberg A
  • Tran T
  • Shacter E
  • Leonardi A
  • Anver M
  • Love P
  • Sher A
  • Siebenlist U

Journal

Immunity

Publication Data

April 13, 1997

Associated Grants

None

Mesh Terms

  • Animals
  • Antibodies, Viral
  • B-Lymphocyte Subsets
  • Cell Differentiation
  • Cell Line
  • Embryo, Mammalian
  • Germinal Center
  • Immunity, Cellular
  • Influenza A virus
  • Mice
  • Mice, Inbred Strains
  • Mice, Knockout
  • Proto-Oncogene Proteins
  • Proto-Oncogenes
  • Spleen
  • Stem Cells
  • T-Lymphocytes
  • Toxoplasmosis
  • Transcription Factors