Siglec-G regulates B1 cell survival and selection

Julia Jellusova, Sandra Düber, Eva Gückel, Christoph J. Binder, Siegfried Weiss, Reinhard Voll, Lars Nitschke

Research output: Contribution to journalArticlepeer-review

49 Scopus citations


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.

Original languageEnglish
Pages (from-to)3277-3284
Number of pages8
JournalJournal of Immunology
Issue number6
StatePublished - 15 Sep 2010
Externally publishedYes


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