First Author | Jellusova J | Year | 2010 |
Journal | J Immunol | Volume | 185 |
Issue | 6 | Pages | 3277-84 |
PubMed ID | 20729333 | Mgi Jnum | J:163534 |
Mgi Id | MGI:4822272 | Doi | 10.4049/jimmunol.1001792 |
Citation | Jellusova J, et al. (2010) Siglec-g regulates b1 cell survival and selection. J Immunol 185(6):3277-84 |
abstractText | Siglec-G is a negative regulator of BCR-mediated signaling in B1a cells. This population of B cells is highly increased in Siglec-G-deficient mice, but the mechanism of this expansion is not known so far. In this study, we demonstrate that Siglecg(-/-) B1a cells show a lower level of spontaneous apoptosis and a prolonged life span. Mechanistically, the lower apoptosis could result from higher expression levels of the transcription factor NFATc1 in Siglec-G-deficient B1a cells. Interestingly, Siglecg(-/-) B1a cells display an altered BCR repertoire compared with wild-type B1a cells. As the BCR repertoire and the VDJ composition of Igs of Siglecg(-/-) B1a cells resembles more the Abs produced by adult bone marrow-derived B cells rather than canonical fetal liver-derived B1a cells, this suggest that the selection into the B1a cell population is altered in Siglec-G-deficient mice. |