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*
Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104; and
Department of Biochemistry, University of Wisconsin, Madison, WI 53706
Peripheral B cells are divided into two subpopulations, B-1 and
B-2, the relationship of which remains obscure. We recently showed that
the Bcmd mutation in A/WySnJ mice reduces average B cell
life span, yielding 90% fewer peripheral B cells. Despite this defect,
A/WySnJ mice have an elevated proportion of peritoneal CD5+
B cells, suggesting that Bcmd may be the first
B-cell-intrinsic gene to differentially affect the B-1 and B-2
subpopulations. To test this hypothesis in detail, we have used in vivo
BrdU labeling and four-color cytofluorometry to examine the numbers and
turnover rates of sIgM+CD23-CD43+
(B-1) and sIgM+CD23+CD43- (B-2)
splenocytes in A/WySnJ and A/J mice. The results show the expected 90%
reduction of splenic B-2 cells among A/WySnJ mice, but a normal splenic
B-1 cell pool. Increased B-1 cell renewal cannot explain this
undiminished pool, because BrdU labeling kinetics reveals an identical
splenic B-1 subset turnover rate of 
4%/day in both A/WySnJ and A/J
strains. Thus, B-1 cells are Bcmd-independent but B-2 cells
are Bcmd-dependent, suggesting Bcmd functions
in a positive signaling pathway that imparts longevity to quiescent B
cells, but that is not required for cycling B cells. Moreover these
results show that the requisites for maturation and longevity differ
between the B-1 and B-2 subsets.
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