| First Author | Eyquem S | Year | 2004 |
| Journal | Eur J Immunol | Volume | 34 |
| Issue | 11 | Pages | 3187-96 |
| PubMed ID | 15384043 | Mgi Jnum | J:93845 |
| Mgi Id | MGI:3505833 | Doi | 10.1002/eji.200425352 |
| Citation | Eyquem S, et al. (2004) The development of early and mature B cells is impaired in mice deficient for the Ets-1 transcription factor. Eur J Immunol 34(11):3187-96 |
| abstractText | The Ets-1 transcription factor is essential for normal development of the natural killer and T cell lineages; however, its role in B cell development remains poorly understood. To address this issue, we used gene targeting to inactivate Ets-1 in mice (Ets-1(-/-)). We show here that the development of B cell precursors, particularly steps requiring pre-B cell receptor function, is defective in Ets-1(-/-) mice. Peripheral B cell subsets were analyzed in RAG2-deficient mice reconstituted with Ets-1(-/-) fetal liver cells. In such Ets-1(-/-) chimeric mice, B cell precursors develop into IgM/IgD-bearing cells, but B-1a cells as well as transitional-2 and marginal zone B cell subsets of the spleen are absent. In response to B cell receptor stimulation, Ets-1(-/-) splenic B cells fail to express the CD69 and CD25 activation markers. Furthermore, despite activation of ERK and JNK signaling pathways, Ets-1-deficient B cells do not proliferate and die following BCR engagement. These findings demonstrate that the effect of Ets-1 inactivation is not restricted to the terminal B cell differentiation stage, but also affects the development and function of earlier B cell subsets. |
