| First Author | Samardzic T | Year | 2002 |
| Journal | Mol Cell Biol | Volume | 22 |
| Issue | 23 | Pages | 8320-31 |
| PubMed ID | 12417733 | Mgi Jnum | J:87400 |
| Mgi Id | MGI:2686825 | Doi | 10.1128/MCB.22.23.8320-8331.2002 |
| Citation | Samardzic T, et al. (2002) BOB.1/OBF.1 deficiency affects marginal-zone B-cell compartment. Mol Cell Biol 22(23):8320-31 |
| abstractText | Marginal-zone (MZ) B cells represent a first line of defense against particulate blood-borne antigens. Together with the B1 cells, they are responsible for the early response against type II T-independent antigens. The molecular pathways controlling the development of MZ B cells are only poorly understood. We found that these cells are virtually absent in mice deficient in the BOB.1/OBF.1 coactivator. Loss of these B cells was demonstrated by the lack of cells showing the appropriate cell surface phenotype but also by histological analyses and tri-nitro-phenol-Ficoll capturing. The lack of these cells is a B-cell-intrinsic defect, as shown by bone marrow complementation experiments. We also show that the expression of BOB.1/OBF.1 in peripheral B cells is required for the development of MZ B lymphocytes. Our analysis of BOB.1/OBF.1-deficient splenic B cells reveals alterations in cell motility, tumor necrosis factor receptor expression, and B-cell receptor (BCR) signaling. These changes could contribute to the loss of MZ B lymphocytes by altering the maturation of the cells. Interestingly, development of and BCR signaling in B1 B cells are completely normal in BOB.1/OBF.1 mutant mice. |
