| First Author | Schmidt NW | Year | 2006 |
| Journal | J Leukoc Biol | Volume | 79 |
| Issue | 4 | Pages | 852-9 |
| PubMed ID | 16461747 | Mgi Jnum | J:107548 |
| Mgi Id | MGI:3621400 | Doi | 10.1189/jlb.0705402 |
| Citation | Schmidt NW, et al. (2006) p53 regulates Btk-dependent B cell proliferation but not differentiation. J Leukoc Biol 79(4):852-9 |
| abstractText | Btk is critical for B cell development and proliferation. Mice lacking Btk have a defect in B cell development, resulting in a loss of mature B cells and decreased proliferative responses following B cell receptor cross-linking. In contrast, mice deficient in the tumor suppressor p53 display increases in developing B cell populations in the bone marrow. To investigate the potential role of p53 in Btk-dependent B cell development and function, we generated mice doubly-deficient in p53 and Btk. Btk/p53-deficient mice showed an increase in splenic B220+ cell numbers compared with Btk-deficient mice, although there was no recovery in B cell subset differentiation. In contrast to the lack of recovery of B cell development, there was a recovery in lipopolysaccharide and anti-immunoglobulin M (IgM) plus interleukin-4-induced proliferation of Btk/p53-deficient B cells, although there was no recovery to anti-IgM stimulation alone. Thus, p53 promotes B cell expansion and proliferation, but p53 deficiency cannot compensate for Btk deficiency in the development of B cell subsets. |
