| First Author | Lentz VM | Year | 1996 |
| Journal | J Immunol | Volume | 157 |
| Issue | 2 | Pages | 598-606 |
| PubMed ID | 8752907 | Mgi Jnum | J:34046 |
| Mgi Id | MGI:81524 | Doi | 10.4049/jimmunol.157.2.598 |
| Citation | Lentz VM, et al. (1996) Bcmd governs recruitment of new B cells into the stable peripheral B cell pool in the A/WySnJ mouse. J Immunol 157(2):598-606 |
| abstractText | The A/WySnJ mouse provides a genetic model for studying new B cell selection into the stable peripheral B cell pool. Unlike the related A/J strain, the A/WySnJ has a single, autosomal codominant gene defect, Bcmd, resulting in a profound peripheral B cell deficiency. Here, continuous in vivo bromodeoxyuridine labeling and immunofluorescence analysis showed normal bone marrow B cell genesis but excessive B cell loss from the marrow and each peripheral pool in A/WySnJ. The A/WySnJ immature B220low/HSAhigh splenic B cell pool was 79% smaller, had a 69% slower renewal rate, and its cells had a 29% shorter average half-life than A/J. The A/WySnJ mature B220high/HSAlow splenic B cell pool was 92% smaller, had an 83% slower renewal rate, and its cells had a 56% shorter average half-life. In reciprocal chimeras, the A/WySnJ marrow failed to repopulate the peripheral B cell pool in A/J mice, whereas the A/J marrow fully reconstituted the A/WySnJ mice. Histochemistry revealed disordered splenic architecture in A/WySnJ, with few primary lymphoid follicles and a second abnormal phenotype, mastocytosis. There was no common genetic basis for B cell deficiency and mastocytosis in the F2 progeny of an (A/WySnJ x CAST/Ei)F1 intercross. We conclude that Bcmd is expressed in bone marrow cells, most likely B cells, where it hinders short-lived B cell maturation to a long-lived phenotype with the potential to form memory B cells. |
