| First Author | Horcher M | Year | 2001 |
| Journal | Immunity | Volume | 14 |
| Issue | 6 | Pages | 779-90 |
| PubMed ID | 11420047 | Mgi Jnum | J:75504 |
| Mgi Id | MGI:2176720 | Doi | 10.1016/s1074-7613(01)00153-4 |
| Citation | Horcher M, et al. (2001) Pax5/BSAP maintains the identity of B cells in late B lymphopoiesis. Immunity 14(6):779-90 |
| abstractText | The B lineage commitment factor Pax5 (BSAP) is expressed throughout B cell development. To investigate its late function, we generated a mouse strain carrying a floxed Pax5 allele that was conditionally inactivated by CD19-cre or Mx-cre expression. Pax5 deletion resulted in the preferential loss of mature B cells, inefficient lymphoblast formation, and reduced serum IgG levels. Mature B cells radically changed their gene expression pattern in response to Pax5 inactivation. Most B cell antigens were downregulated on the cell surface, and the transcription of B cell-specific genes was decreased, whereas the expression of non-B lymphoid genes was activated in Pax5-deficient B cells. These data demonstrate that Pax5 is essential for maintaining the identity and function of B cells during late B lymphopoiesis. |
