| First Author | Zhu X | Year | 2008 |
| Journal | Eur J Immunol | Volume | 38 |
| Issue | 9 | Pages | 2587-99 |
| PubMed ID | 18792411 | Mgi Jnum | J:141226 |
| Mgi Id | MGI:3817791 | Doi | 10.1002/eji.200838323 |
| Citation | Zhu X, et al. (2008) Transgenic expression of Spi-C impairs B-cell development and function by affecting genes associated with BCR signaling. Eur J Immunol 38(9):2587-99 |
| abstractText | Spi-C is an Ets family transcription factor closely related to PU.1 and Spi-B. Expression of Spi-C is developmentally regulated in the B-cell lineage, but its function remains unknown. To determine the function of Spi-C in B-cell development, we generated mice expressing a B-cell-specific Spi-C transgene under the control of the IgH intronic enhancer. Spi-C transgenic mice had 50% fewer B cells than wild-type littermates. Flow cytometric analyses showed that splenic transitional B cells and bone marrow pre-B or immature B cells from transgenic mice were dramatically reduced compared with those of wild type. Both nonspecific and Ag-specific serum IgM levels were significantly increased in transgenic mice, while serum IgG levels were significantly decreased compared with wild type. Spi-C transgenic B cells proliferated poorly after stimulation by anti-IgM or anti-CD40 in vitro, although they responded normally to LPS stimulation. Using real-time RT-PCR, we found that several BCR signaling-related mediators were downregulated at pre-B-cell and mature B-cell stages in transgenic mice, while an inhibitor of BCR signaling was upregulated. Taken together, these data indicate that ectopic expression of Spi-C can impair B-cell development and function by affecting genes associated with BCR signaling. |
