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Publication : Siglec-G regulates B1 cell survival and selection.

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.
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