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Julia Jellusova, Sandra Düber, Eva Gückel, Christoph J Binder, Siegfried Weiss, Reinhard Voll, Lars Nitschke, Siglec-G Regulates B1 Cell Survival and Selection, The Journal of Immunology, Volume 185, Issue 6, September 2010, Pages 3277–3284, https://doi.org/10.4049/jimmunol.1001792
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Abstract
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.