First Author | Thomas MD | Year | 2005 |
Journal | Immunity | Volume | 23 |
Issue | 3 | Pages | 275-86 |
PubMed ID | 16169500 | Mgi Jnum | J:113271 |
Mgi Id | MGI:3665339 | Doi | 10.1016/j.immuni.2005.08.005 |
Citation | Thomas MD, et al. (2005) c-Myb is critical for B cell development and maintenance of follicular B cells. Immunity 23(3):275-86 |
abstractText | The c-Myb transcription factor is crucial during definitive hematopoiesis. However, the embryonic lethality of Myb traditional null mutations has precluded analysis of c-Myb function in lymphocytes. Using tissue-specific inactivation at the Myb locus, we demonstrate that loss of Myb causes a partial block during B cell development at the pro-B to pre-B cell transition, resulting in greatly decreased output of new B cells from the bone marrow. Furthermore, we demonstrate that Myb is not essential for the proliferation of splenic B cells, but that loss of c-Myb function prevents normal B cell homeostasis due to decreased splenic B cell survival. Decreased survival is accompanied by hyporesponsiveness to the B cell survival factor BLyS (also termed BAFF), decreased expression of the BLyS receptor 3 (BR3), and altered regulation of PKCdelta nuclear accumulation. Thus, c-Myb is important during multiple stages of B-lymphopoiesis. |