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Updated: Aug 16, 2026

Murine Model of CD40-activation of B cells
Published on: March 6, 2010
IL-10 production and CD40L expression in patients with common variable immunodeficiency
1Department of Allergy and Clinical Immunology, La Sapienza University of Rome, Italy.
Insights
Common variable immunodeficiency (CVI) patients show normal interleukin-10 (IL-10) production, but CD40 ligand (CD40L) expression may be functionally defective in some cases, impacting IgG production.
Area of Science:
- Immunology
- Clinical Medicine
- Molecular Biology
Background:
- Common variable immunodeficiency (CVI) is characterized by impaired antibody production.
- The roles of CD40 ligand (CD40L) and interleukin-10 (IL-10) in CVI pathogenesis are not fully understood.
Purpose of the Study:
- To investigate CD40L expression and IL-10 production in CVI patients.
- To determine the potential contribution of these factors to impaired IgG production in CVI.
Main Methods:
- Flow cytometry was used to measure CD40L expression on peripheral blood mononuclear cells (PBMCs) from CVI patients and controls.
- IL-10 production was assessed after in vitro stimulation of PBMCs.
- In vitro IgG production was induced using anti-CD40 and cytokine stimulation.
Main Results:
- CD40L expression was comparable to controls in most CVI patients, but functional defects were observed in some.
- IL-10 production was similar in CVI patients and controls.
- In vitro stimulation induced significant IgG production in only one of 13 CVI patients tested.
Conclusions:
- Altered IL-10 production is unlikely to be a major factor in impaired IgG production in most CVI patients.
- While CD40L is often normally expressed, functional defects may contribute to CVI in a subset of patients.
- Further research is needed to elucidate the precise mechanisms underlying CVI pathogenesis.
Abstract:
The authors studied CD40 ligant (CD40L) expression and interleukin-10 (IL-10) production in 16 patients with common variable immunodeficiency (CVI). Mean CD40L expression, determined by using cytofluorimetry, and measured as the mean fluorescence intensity following stimulation of peripheral blood mononuclear cells (PBMC) with phorbol myristate acetate (PMA) and calcium ionophore in 12 patients, was comparable to that of controls. However, three CVI patients showed fluorescence intensity in stimulated cells below 2 standard deviations of normal donors' mean and two other patients had only a slight increase of stimulated versus unstimulated cells (< 10 channels). IL-10 production after stimulation of PBMC with both anti-CD3 or anti-CD3 plus PMA gave similar results in CVI patients and normal controls. In vitro stimulation of PBMC with anti-CD40 and various combinations of cytokines (IL-2, IL-4 and IL-10) induced IgG production above 100 ng/ml in one CVI patient out of 13 tested. The data suggest that alterations of IL-10 production are unlikely to play a major role in the pathogenesis of impaired IgG production in most CVI patients. CD40L appears to be normally expressed in two thirds of CVI patients, but it may be functionally defective.
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