| First Author | Lentz VM | Year | 1998 |
| Journal | J Immunol | Volume | 160 |
| Issue | 8 | Pages | 3743-7 |
| PubMed ID | 9558076 | Mgi Jnum | J:46943 |
| Mgi Id | MGI:1202259 | Doi | 10.4049/jimmunol.160.8.3743 |
| Citation | Lentz VM, et al. (1998) Bcmd decreases the life span of B-2 but not B-1 cells in A/WySnJ mice. J Immunol 160(8):3743-7 |
| abstractText | 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 tells, 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 similar to 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. |
