Jellusova J, Dueber S, Gueckel E, Binder CJ, Weiss S, Voll R, Nitschke L (2010)
Publication Status: Published
Publication Type: Journal article
Publication year: 2010
Publisher: AMER ASSOC IMMUNOLOGISTS
Book Volume: 185
Pages Range: 3277-3284
Journal Issue: 6
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. The Journal of Immunology, 2010, 185: 3277-3284.
APA:
Jellusova, J., Dueber, S., Gueckel, E., Binder, C.J., Weiss, S., Voll, R., & Nitschke, L. (2010). Siglec-G Regulates B1 Cell Survival and Selection. Journal of Immunology, 185(6), 3277-3284. https://doi.org/10.4049/jimmunol.1001792
MLA:
Jellusova, Julia, et al. "Siglec-G Regulates B1 Cell Survival and Selection." Journal of Immunology 185.6 (2010): 3277-3284.
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