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Review
. 2008 Aug-Sep;86(6):485-6.
doi: 10.1038/icb.2008.35. Epub 2008 May 20.

B cell survival: an unexpected mechanism of lymphocyte vitality

Micah J Benson  1 , Raul Elgueta, Randolph J Noelle
Affiliations
Review

B cell survival: an unexpected mechanism of lymphocyte vitality

Micah J Benson et al. Immunol Cell Biol. 2008 Aug-Sep.
No abstract available

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Figures

Figure 1
Figure 1
TRAF2 and TRAF3 cooperatively and constitutively repress the alternative NF-κB pathway, with BAFF-R signaling relieving this suppression. In all reports describing deficient BAFF-R signaling, blunted naive mature B cell survival and development is the result (a). When BAFF-R signaling is deficient, TRAF3 and TRAF2 cooperate to constitutively degrade NIK and thus block activation of the alternative NK-κB pathway (a). It is thought that both TRAF2 and TRAF3 bind to NIK and cooperate in its degradation, with the heterocomplex of TRAF2/TRAF3/NIK depicted in (a) purely hypothetical. Upon ligation of BAFF-R by BAFF (b), TRAF3 is recruited to an atypical TRAF3-binding site located in the cytoplasmic tail of BAFF-R (depicted by the amino acid sequence PVPAT). TRAF3 is then targeted for degradation in a TRAF2-dependent manner. Owing to depleted TRAF3 levels, NIK is no longer the subject of continual degradation and can activate the alternative NF-κB pathway. Through NF-κB2 signaling, B cell survival and the transitional B cell developmental checkpoints occur.
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