Mice lacking the c-rel proto-oncogene exhibit defects in lymphocyte proliferation, humoral immunity, and interleukin-2 expression

Frank Köntgen, Raelene J. Grumont, Andreas Strasser, Donald Metcalf, Ruili Li, David Tarlinton, Steve Gerondakis

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The c-rel proto-oncogene, which is expressed predominantly in hemopoietic cells encodes a subunit of the NF-κB-like family of transcription factors. In mice with an inactivated c-rel gene, whereas development of cells from all hemopoietic lineages appeared normal, humoral immunity was impaired and mature B and T cells were found to be unresponsive to most mitogenic stimuli. Phorbol ester and calcium ionophore costimulation, in contrast to certain membrane receptor-mediated signals, overcame the T cell-proliferative defect, demonstrating that T cell proliferation occurs by Rel-dependent and - independent mechanisms. The ability of exogenous interleukin-2 to restore T cell, but not B cell, proliferation indicates that Rel regulates the expression of different genes in B and T cells that are crucial for cell division and immune function.

Original languageEnglish
Pages (from-to)1965-1977
Number of pages13
JournalGenes & Development
Issue number16
Publication statusPublished - 15 Aug 1995
Externally publishedYes


  • autoregulation
  • cytokine
  • lymphocyte proliferation
  • NF-κB
  • Protooncogene
  • transcription factor

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