| First Author | Ye M | Year | 2005 |
| Journal | J Exp Med | Volume | 202 |
| Issue | 10 | Pages | 1411-22 |
| PubMed ID | 16301746 | Mgi Jnum | J:118844 |
| Mgi Id | MGI:3700458 | Doi | 10.1084/jem.20051089 |
| Citation | Ye M, et al. (2005) PU.1 is not strictly required for B cell development and its absence induces a B-2 to B-1 cell switch. J Exp Med 202(10):1411-22 |
| abstractText | In this paper, we describe the unexpected outgrowth of B lineage cells from PU.1(-/-) fetal liver cultures. The cells express all early B cell genes tested, including the putative PU.1 target genes IL-7R and EBF but not B220, and can produce immunoglobulin M. However, we observed a delay in the PU.1(-/-) B cell outgrowth and reduced precursor frequencies, indicating that although PU.1 is not strictly required for B cell commitment, it facilitates B cell development. We also ablated PU.1 in CD19-expressing B lineage cells in vivo, using a Cre-lox approach that allows them to be tracked. PU.1 excision resulted in a shift from B-2 cells to B-1-like cells, which dramatically increased with the age of the mice. Our data indicate that this shift is predominantly caused by a B-2 to B-1 cell reprogramming. Furthermore, we found that B-2 cells express substantially more PU.1 than B-1 cells, which is consistent with the idea that maintenance of the B-2 cell phenotype requires relatively high levels of PU.1, but B-1 cells require little. |
