| First Author | Hesslein DG | Year | 2006 |
| Journal | Mol Immunol | Volume | 43 |
| Issue | 4 | Pages | 326-34 |
| PubMed ID | 16310046 | Mgi Jnum | J:104843 |
| Mgi Id | MGI:3612908 | Doi | 10.1016/j.molimm.2005.02.010 |
| Citation | Hesslein DG, et al. (2006) Origins of peripheral B cells in IL-7 receptor-deficient mice. Mol Immunol 43(4):326-34 |
| abstractText | The interleukin 7 (IL-7) signaling pathway is critical for early lymphoid differentiation. We found dramatic perturbations in fetal liver B cell development and confirmed a complete absence of developing B cells in the adult bone marrow in mice lacking the IL-7 receptor alpha (IL-7Ralpha) gene. We show that peripheral B-2 and B-1 cell populations are deficient in IL-7Ralpha-/- mice. B-2 follicular cell and peritoneal B-1 cell percentages are reduced, while B-2 marginal zone cell percentages are increased. A comparison of bone marrow and splenic populations at different ages revealed that the splenic B cell populations seen in adult IL-7Ralpha-/- mice first appear during neonatal development. We have measured N-nucleotide addition at the joints of V(D)J rearrangements in splenic B cells and have used it as a somatic marker to define and separate bone marrow-derived B cells from fetal liver-derived B cells. B cells isolated from the bone marrow and spleen of adult and neonatal IL-7Ralpha-deficient mice harbor high levels of N-nucleotide additions similar to those found in equivalent wild-type B cell populations. We conclude that the majority of splenic B cells in IL-7Ralpha-deficient mice originate from the bone marrow and not the fetal liver. |
