TRAF2 and TRAF3 signal adapters act cooperatively to control the maturation and survival signals delivered to B cells by the BAFF receptor.
Immunity, 2008/3;28(3):391-401.
Gardam S[1], Sierro F, Basten A, Mackay F, Brink R
Affiliations
PMID: 18313334DOI: 10.1016/j.immuni.2008.01.009
Impact factor: 43.474
Abstract
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.
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
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