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Decreased CD3-mediated interferon-gamma production in relapsing-remitting multiple sclerosis
1Department of Neurology, University of Texas-Houston Health Science Center 77225, USA.
Annals of Neurology
|April 1, 1995
Summary
Multiple sclerosis (MS) patients exhibit impaired T-cell responses, specifically a reduced response to anti-CD3 antibody stimulation. This suggests a potential defect in T-cell receptor signaling and interferon-gamma secretion in MS.
Area of Science:
- Immunology
- Neuroscience
- Cell Biology
Background:
- Multiple sclerosis (MS) is a chronic central nervous system inflammatory disease.
- T-cell mediation is a proposed mechanism underlying MS pathogenesis.
Purpose of the Study:
- To investigate T-cell proliferation and cytokine secretion in relapsing-remitting MS patients.
- To compare immune responses in MS patients versus healthy controls following specific stimulations.
Main Methods:
- Mononuclear cells from MS patients and controls were stimulated with OKT3 (anti-CD3) antibody, concanavalin A, or ionomycin/PMA.
- Proliferation assays and cytokine secretion (interferon-gamma, TGF-beta, IL-10, TNF-alpha, IL-2, IL-4) were measured.
Main Results:
- MS patients showed significantly decreased proliferation and interferon-gamma secretion upon anti-CD3 stimulation compared to controls.
- No significant differences were observed in responses to concanavalin A or ionomycin/PMA.
- Transforming growth factor-beta secretion was significantly increased in MS patients after anti-CD3 stimulation.
Conclusions:
- A potential abnormality in T-cell receptor signal transduction exists in MS.
- Impaired interferon-gamma secretion via the CD3 T-cell receptor complex may contribute to MS pathophysiology.