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Updated: Aug 8, 2026
Detection of True IgE-expressing Mouse B Lineage Cells
Published on: December 1, 2014
Negative feedback regulation of IgE synthesis by murine CD23
P Yu1, M Kosco-Vilbois, M Richards
1Max-Planck-Institut für Immunbiologie, Freiburg, Germany.
Insights
Murine CD23 deficiency does not affect B- and T-cell development or parasitic immune responses. However, CD23-deficient mice show increased immunoglobulin E (IgE) antibody production to thymus-dependent antigens, suggesting CD23 negatively regulates IgE.
Area of Science:
- Immunology
- Molecular Biology
Background:
- Immunoglobulin E (IgE) plays a crucial role in parasitic infections and allergic reactions.
- CD23, the low-affinity IgE receptor (Fc epsilon RII), is implicated in regulating IgE synthesis.
- Murine CD23 is expressed on B cells and follicular dendritic cells; human CD23 exists in two forms with varied expression.
Purpose of the Study:
- To investigate the in vivo function of CD23 in regulating IgE synthesis and immune responses.
- To clarify the role of CD23 in B- and T-cell development and immune responses to parasitic and thymus-dependent antigens.
Main Methods:
- Gene disruption of murine CD23 to create CD23-deficient mice.
- Assessment of B- and T-cell development in CD23-deficient mice.
- Evaluation of immune responses to the helminth Nippostrongylus brasiliensis and thymus-dependent antigens.
Main Results:
- CD23-deficient mice exhibit normal B- and T-cell development.
- Immune responses to Nippostrongylus brasiliensis are unaffected in the absence of CD23.
- Mice lacking CD23 demonstrate elevated and prolonged specific IgE antibody titers following immunization with thymus-dependent antigens.
Conclusions:
- Murine CD23 functions as a negative feedback regulator of IgE production.
- The absence of CD23 leads to dysregulated IgE responses, particularly to thymus-dependent antigens.
Abstract:
Immunoglobulin E is found in nanogram amounts in normal human and mouse serum. It is increased during parasitic infestations and mediates allergy. CD23, the low-affinity receptor for IgE (Fc epsilon RII), has been proposed as an important regulator of IgE synthesis. The type-II transmembrane lectin CD23 is expressed in the mouse on B cells and follicular dendritic cells. In humans there are two forms of CD23 which differ in their intracellular amino-terminal 6/7 amino acids; expression of the A-form corresponds to that of murine CD23, whereas the B-form is also found on T and other haematopoietic cells. CD23 has been implicated in cellular adhesion, antigen presentation, as a growth and differentiation factor for human B, T and plasma cells, and as a signal transduction molecule (reviewed in refs 3, 8). Here we disrupt the gene coding for murine CD23 (ref. 9) to clarify the role of CD23 in vivo and find that B- and T-cell development is normal in these CD23-deficient mice. Immune responses to the helminth Nippostrongylus brasiliensis are unaffected. In contrast, immunization with thymus-dependent antigens leads to increased and sustained specific IgE antibody titres compared with controls. Formation of germinal centres is normal. These results suggest that murine CD23 acts as a negative feedback component of IgE regulation.
