| First Author | Schubart DB | Year | 2000 |
| Journal | J Immunol | Volume | 164 |
| Issue | 1 | Pages | 18-22 |
| PubMed ID | 10604987 | Mgi Jnum | J:59109 |
| Mgi Id | MGI:1350909 | Doi | 10.4049/jimmunol.164.1.18 |
| Citation | Schubart DB, et al. (2000) Cutting edge: lack of peripheral B cells and severe agammaglobulinemia in mice simultaneously lacking Bruton's tyrosine kinase and the B cell-specific transcriptional coactivator OBF-1. J Immunol 164(1):18-22 |
| abstractText | OBF-1 is a B cell-restricted transcriptional coactivator that is recruited to octamer-containing promoters by interacting with the POU domain of Oct-1 or Oct-2. We have shown earlier that mice lacking OBF-1 were dramatically impaired in their ability to mount humoral immune responses and did not develop germinal centers in the spleen; however, they had a largely normal B cell development in the bone marrow. In this study, we demonstrate that OBF-1-deficient mice also have an early defect in B cell development and show that OBF-1-/- immature B cells are greatly impaired at the transition from the bone marrow to the spleen. In addition, when the OBF-1 mutation is combined to a mutation in the gene encoding Bruton's tyrosine kinase, a striking phenotype is observed. These double-deficient animals lack peripheral B cells and have virtually no serum Igs, thus closely resembling human X chromosome-linked agammaglobulinemia. |
