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Updated: Aug 2, 2026
Murine Model of CD40-activation of B cells
Published on: March 6, 2010
Differential control of CD22 ligand expression on B and T lymphocytes, and enhanced expression in murine systemic
Frédéric Lajaunias1, Akinori Ida, Shuichi Kikuchi
1Department of Pathology, University of Geneva, Geneva, Switzerland.
Insights
CD22 ligand (CD22L) expression differs between B and T cells. Increased CD22L on circulating B cells indicates severe systemic lupus erythematosus (SLE) progression, suggesting CD22-CD22L interactions are key in SLE and humoral immunity.
Area of Science:
- Immunology
- Molecular Biology
- Autoimmunity
Background:
- CD22 is a B cell glycoprotein regulating B cell receptor signaling.
- CD22 interacts with alpha2,6-linked sialic acid-bearing glycans (CD22 ligands).
- CD22 ligands are expressed on B and T cells, influencing immune responses.
Purpose of the Study:
- Investigate CD22 ligand (CD22L) expression modulation in lymphocytes.
- Determine CD22L expression changes upon lymphocyte activation.
- Correlate CD22L expression with systemic lupus erythematosus (SLE) progression.
Main Methods:
- Flow cytometry assessed CD22L expression on B and T cells in mice.
- Lymphocytes were stimulated in vitro with antigens or mitogens.
- CD22L levels on circulating lymphocytes were correlated with SLE severity in lupus-prone mice.
Main Results:
- CD22L constitutively expressed on mature B cells, not T cells, in nonautoimmune mice.
- Antigen stimulation upregulated CD22L on T cells; polyclonal activation upregulated CD22L on B cells.
- Increased CD22L on circulating B and T cells correlated with SLE progression in lupus-prone mice.
Conclusions:
- CD22L expression is differentially regulated in B and T cells.
- High CD22L on circulating B cells marks severe SLE development.
- CD22-CD22L interactions likely play a role in SLE and humoral immunity regulation.
Objective:
CD22, a B cell-restricted transmembrane glycoprotein, regulates B cell antigen receptor signaling upon interaction with alpha2,6-linked sialic acid-bearing glycans, which act as ligands and are expressed on B and T cells. In this study, we investigated how the expression of CD22 ligand (CD22L) is modulated following lymphocyte activation or during the course of systemic lupus erythematosus (SLE).
Methods:
The expression levels of CD22L on B and T cells in nonautoimmune mice were assessed by flow cytometric analysis using a soluble recombinant form of CD22, following stimulation with antigen or mitogen in vitro. In addition, the expression levels of CD22L on circulating lymphocytes were correlated with the progression of SLE in lupus-prone mice.
Results:
We observed a constitutive expression of CD22L on mature B cells, but not T cells, in nonautoimmune mice. However, CD22L levels were up-regulated selectively on T cells (but not B cells) stimulated with antigens in vitro, while their expression levels on B cells was up-modulated following polyclonal activation with lipopolysaccharide. Furthermore, expression of CD22L was increased on circulating B cells (and to a lesser extent on T cells) in parallel with progression of SLE in several different lupus-prone mice and in a cohort of (C57BL/6 x [NZB x C57BL/6.Yaa]F(1)) backcross mice.
Conclusion:
The expression of CD22L is differentially regulated in B and T cells, and high expression of CD22L on circulating B cells is a marker for development of severe SLE, suggesting a role for CD22-CD22L interactions in SLE as well as in the regulation of humoral immunity.
