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Transgene CD23 expression on lymphoid cells modulates IgE and IgG1 responses
1Department of Molecular Cell Biology/Central Nervous System, Ciba-Geigy Limited, Basel, Switzerland.
Journal of Immunology (Baltimore, Md. : 1950)
|October 1, 1994
Summary
Overexpressing transmembrane CD23 (mCD23) in mice impairs immune responses, specifically reducing IgE and IgG1 production, without affecting lymphoid cell development.
Area of Science:
- Immunology
- Molecular Biology
- Transgenic Models
Background:
- CD23 exists in transmembrane (mCD23) and soluble (sCD23) forms, involved in immune functions.
- Abnormal CD23 expression is linked to lymphoid cell pathologies.
- Understanding CD23's role in vivo requires studying its overexpression effects.
Purpose of the Study:
- To investigate the in vivo effects of mCD23 and sCD23 overexpression on lymphoid cell development and immune function.
- To determine if CD23 overexpression impacts B and T cell maturation and antibody production.
Main Methods:
- Generation of transgenic mice overexpressing either mCD23 or sCD23 under Thy-1 and Ig heavy chain enhancer control.
- Analysis of lymphoid cell populations in thymus, spleen, bone marrow, and lymph nodes.
- Assessment of serum IgE and IgG1 levels during experimental immune responses.
- In vitro IgE and IgG1 secretion assays using B cells from transgenic mice.
Main Results:
- mCD23 and sCD23 overexpression did not significantly alter lymphoid cell maturation or basal IgE/IgG1 levels.
- mCD23 transgenic mice showed impaired increases in serum polyclonal IgE and IgG1 levels in immune response models.
- In vitro, B cells from mCD23 mice secreted normal IgE and IgG1, suggesting intact T-B cell interactions.
Conclusions:
- mCD23 overexpression, but not sCD23, impairs specific antibody production in vivo.
- The findings suggest mCD23-expressing cells influence Ig production through mechanisms beyond direct T-B cell contact.
- Further research is needed to elucidate the precise role of mCD23 in regulating immune responses.