Deficient Fas expression by CD4+ CCR5+ T cells in multiple sclerosis
Eva Julià1, Xavier Montalban, Hammad Al-Zayat
1Unitat de Neuroimmunologia Clínica, Hospital Universitari Vall d'Hebron, Universitat Autònoma de Barcelona, Barcelona, Spain.
Journal of Neuroimmunology
|August 11, 2006
Summary
T cells expressing CCR5 and CXCR3 in multiple sclerosis (MS) patients show reduced Fas expression, potentially increasing their survival and CNS migration. This finding suggests a mechanism contributing to MS pathogenesis.
Area of Science:
- Immunology
- Neuroscience
- Cell Biology
Background:
- Multiple sclerosis (MS) is a chronic inflammatory disease of the central nervous system (CNS).
- T cell infiltration into the CNS is a hallmark of MS pathogenesis.
- Specific T cell subsets, characterized by chemokine receptor expression (CCR5 and CXCR3), are implicated in MS.
Purpose of the Study:
- To investigate the apoptosis resistance of T cells expressing CCR5 and CXCR3 in patients with multiple sclerosis.
- To compare these T cells with those from healthy controls.
Main Methods:
- Flow cytometry was used to analyze the expression of apoptosis-related molecules (Fas, FasL, bcl-2, bax) and activation markers (CD69, TNF-R1).
- Analysis was performed on CD4+ and CD8+ T cells expressing CCR5 and CXCR3.
- The study included 41 MS patients and 12 healthy controls.
Main Results:
- In MS patients, CD4+ T cells expressing CCR5 showed increased CD69 expression, indicating activation.
- Conversely, Fas expression was decreased in these activated CD4+ CCR5+ T cells from MS patients compared to controls.
- No significant differences were noted in other investigated markers within these specific T cell subsets.
Conclusions:
- Reduced Fas expression on activated CD4+ CCR5+ T cells in MS patients may enhance their survival.
- This prolonged survival could facilitate the migration of these T cells into the CNS.
- These findings suggest a potential mechanism by which specific T cell populations contribute to the pathogenesis of multiple sclerosis.
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