| First Author | Quong MW | Year | 2004 |
| Journal | J Exp Med | Volume | 199 |
| Issue | 8 | Pages | 1101-12 |
| PubMed ID | 15078898 | Mgi Jnum | J:91042 |
| Mgi Id | MGI:3045823 | Doi | 10.1084/jem.20031180 |
| Citation | Quong MW, et al. (2004) Receptor Editing and Marginal Zone B Cell Development Are Regulated by the Helix-Loop-Helix Protein, E2A. J Exp Med 199(8):1101-12 |
| abstractText | Previous studies have indicated that the E2A gene products are required to initiate B lineage development. Here, we demonstrate that E2A(+/-) B cells that express an autoreactive B cell receptor fail to mature due in part to an inability to activate secondary immunoglobulin (Ig) light chain gene rearrangement. Both RAG1/2 gene expression and RS deletion are severely defective in E2A(+/-) mice. Additionally, we demonstrate that E2A(+/-) mice show an increase in the proportion of marginal zone B cells with a concomitant decrease in the proportion of follicular B cells. In contrast, Id3-deficient splenocytes show a decline in the proportion of marginal zone B cells. Based on these observations, we propose that E-protein activity regulates secondary Ig gene rearrangement at the immature B cell stage and contributes to cell fate determination of marginal zone B cells. Additionally, we propose a model in which E-proteins enforce the developmental checkpoint at the immature B cell stage. |
