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Updated: Aug 8, 2026

Murine Model of CD40-activation of B cells
Published on: March 6, 2010
Differentially regulated expression and function of CD22 in activated B-1 and B-2 lymphocytes
Frédéric Lajaunias1, Lars Nitschke, Thomas Moll
1Department of Pathology, University of Geneva, Geneva, Switzerland.
Insights
CD22 protein expression differs between B-1 and B-2 cells following activation. B-2 cells down-regulate CD22 upon BCR cross-linking, while B-1 cells show differential regulation, impacting innate and adaptive immunity.
Area of Science:
- Immunology
- Cell Biology
Background:
- CD22 is a B cell-specific protein regulating B cell receptor (BCR) signaling.
- The regulation of CD22 expression in activated B cells remains poorly understood.
Purpose of the Study:
- To investigate the differential regulation of CD22 expression in B-1 and B-2 cells after activation.
- To elucidate the role of CD22 in BCR signaling in different B cell subsets.
Main Methods:
- Flow cytometry to analyze CD22 expression levels.
- Stimulation of B cells with anti-IgM mAb, LPS, anti-CD40 mAb, IL-4, and CpG oligonucleotides.
- Studies in CD22-deficient mice.
Main Results:
- CD22 expression is down-regulated in B-2 cells after BCR cross-linking but up-regulated by LPS, anti-CD40, or IL-4.
- CD22 expression in B-1 cells is minimally affected by anti-IgM but down-regulated by LPS or CpG.
- CD22 plays a limited role in BCR signaling in B-1 cells compared to B-2 cells.
Conclusions:
- CD22 expression and function are differentially regulated in B-1 and B-2 cells.
- These differences may contribute to the distinct roles of B-1 and B-2 cells in innate and adaptive immunity.
Abstract:
CD22 is a B cell-restricted transmembrane protein that apparently controls signal transduction thresholds initiated through the B cell Ag receptor (BCR) in response to Ag. However, it is still poorly understood how the expression of CD22 is regulated in B cells after their activation. Here we show that the expression levels of CD22 in conventional B-2 cells are markedly down-regulated after cross-linking of BCR with anti-IgM mAb but are up-regulated after stimulation with LPS, anti-CD40 mAb, or IL-4. In contrast, treatment with anti-IgM mAb barely modulated the expression levels of CD22 in CD5(+) B-1 cells, consistent with a weak Ca(2+) response in anti-IgM-treated CD5(+) B-1 cells. Moreover, in CD22-deficient mice, anti-IgM treatment did not trigger enhanced Ca(2+) influx in CD5(+) B-1 cells, unlike CD22-deficient splenic B-2 cells, suggesting a relatively limited role of CD22 in BCR signaling in B-1 cells. In contrast, CD22 levels were markedly down-regulated on wild-type B-1 cells in response to LPS or unmethylated CpG-containing oligodeoxynucleotides. These data indicate that the expression and function of CD22 are differentially regulated in B-1 and conventional B-2 cells, which are apparently implicated in innate and adaptive immunity, respectively.
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