| First Author | Berland R | Year | 2003 |
| Journal | Proc Natl Acad Sci U S A | Volume | 100 |
| Issue | 23 | Pages | 13459-64 |
| PubMed ID | 14595020 | Mgi Jnum | J:86543 |
| Mgi Id | MGI:2680742 | Doi | 10.1073/pnas.2233620100 |
| Citation | Berland R, et al. (2003) Normal B-1a cell development requires B cell-intrinsic NFATc1 activity. Proc Natl Acad Sci U S A 100(23):13459-64 |
| abstractText | B-1a cells, an anatomically, phenotypically, and functionally distinct subset of B cells that produce the bulk of natural serum IgM and much of gut-associated IgA, are an important component of the early response to pathogens. Because the induced expression of CD5, a hallmark of B-1a cells, requires a nuclear factor of activated T cells (NFAT)-dependent enhancer, we examined the role of NFAT transcription factors in B-1a development. Here we show that the B-1a compartment is normal in mice lacking NFATc2 but essentially absent in mice lacking NFATc1. Loss of NFATc1 affects both peritoneal and splenic B-1a cells. Because there is a loss of B-1 cells defined by markers other than CD5, NFATc1 is not required simply for CD5 expression on B-1a cells. Using mixed-allotype chimeras and retroviral-mediated gene transduction we show that the requirement for NFATc1 is B cell-intrinsic. We also demonstrate that NFATc1 protein expression is elevated approximately 5-fold in B-1a cells compared with B-2 cells. This is the first definitive demonstration of a B cell-intrinsic function for an NFAT family transcription factor. |
