| First Author | Casola S | Year | 2004 |
| Journal | Nat Immunol | Volume | 5 |
| Issue | 3 | Pages | 317-27 |
| PubMed ID | 14758357 | Mgi Jnum | J:88472 |
| Mgi Id | MGI:3033504 | Doi | 10.1038/ni1036 |
| Citation | Casola S, et al. (2004) B cell receptor signal strength determines B cell fate. Nat Immunol 5(3):317-27 |
| abstractText | B cell receptor (BCR)-mediated antigen recognition is thought to regulate B cell differentiation. BCR signal strength may also influence B cell fate decisions. Here, we used the Epstein-Barr virus protein LMP2A as a constitutively active BCR surrogate to study the contribution of BCR signal strength in B cell differentiation. Mice carrying a targeted replacement of Igh by LMP2A leading to high or low expression of the LMP2A protein developed B-1 or follicular and marginal zone B cells, respectively. These data indicate that BCR signal strength, rather than antigen specificity, determines mature B cell fate. Furthermore, spontaneous germinal centers developed in gut-associated lymphoid tissue of LMP2A mice, indicating that microbial antigens can promote germinal centers independently of BCR-mediated antigen recognition. |
