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TRAF2 and TRAF3 signal adapters act cooperatively to control the maturation and survival signals delivered to B cells by the BAFF receptor.

Tumor necrosis factor receptor-associated factors 2 and 3 (TRAF2 and TRAF3) were shown to function in a cooperative and nonredundant manner to suppress nuclear factor-kappaB2 (NF-kappaB2) activation, gene expression, and survival in mature B cells. In the absence of this suppressive activity, B cells developed independently of the obligatory B cell survival factor, BAFF (B cell-activating factor of the tumor necrosis factor family). However, deletion of either TRAF2 or TRAF3 from the T cell lineage did not promote T cell survival, despite causing extensive NF-kappaB2 activation. This constitutive, lineage-specific suppression of B cell survival by TRAF2 and TRAF3 determines the requirement for BAFF to sustain B cell development in vivo. Binding of BAFF to BAFF receptor reversed TRAF2-TRAF3-mediated suppression of B cell survival by triggering the depletion of TRAF3 protein. This process was TRAF2 dependent, revealing dual roles for TRAF2 in regulating B cell homeostasis.

Pubmed ID: 18313334

Authors

  • Gardam S
  • Sierro F
  • Basten A
  • Mackay F
  • Brink R

Journal

Immunity

Publication Data

March 17, 2008

Associated Grants

None

Mesh Terms

  • Animals
  • B-Cell Activation Factor Receptor
  • B-Lymphocytes
  • Cell Differentiation
  • Cell Survival
  • Flow Cytometry
  • Gene Expression
  • Gene Expression Profiling
  • Mice
  • Mice, Transgenic
  • Oligonucleotide Array Sequence Analysis
  • Phenotype
  • Signal Transduction
  • TNF Receptor-Associated Factor 2
  • TNF Receptor-Associated Factor 3