Enforced bcl-xL gene expression restored splenic B lymphocyte development in BAFF-R mutant mice

IJ Amanna, JP Dingwall, CE Hayes - The Journal of Immunology, 2003 - journals.aai.org
IJ Amanna, JP Dingwall, CE Hayes
The Journal of Immunology, 2003journals.aai.org
The TNFR family member BAFF-R facilitates peripheral B cell development, although it is
unclear whether it promotes survival of B cells, or also initiates a differentiation program. We
show that disruption of the BAFF-R encoding gene Tnfrsf13c in strain A/WySnJ mice causes
a progressive decline in peripheral B cell numbers, beginning at the transitional 1
developmental stage and continuing through the mature peripheral B cell stage. Bcl-x L
overexpression in A/WySnJ B cells decreased the turnover of transitional B cells, as …
Abstract
The TNFR family member BAFF-R facilitates peripheral B cell development, although it is unclear whether it promotes survival of B cells, or also initiates a differentiation program. We show that disruption of the BAFF-R encoding gene Tnfrsf13c in strain A/WySnJ mice causes a progressive decline in peripheral B cell numbers, beginning at the transitional 1 developmental stage and continuing through the mature peripheral B cell stage. Bcl-x L overexpression in A/WySnJ B cells decreased the turnover of transitional B cells, as determined by 5-bromo-2′-deoxyuridine labeling, and restored follicular B cell development. We conclude that the mutant A/WySnJ allele of Tnfrsf13c can be complemented through the survival signal provided by Bcl-x L.
journals.aai.org