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Monocyte-derived cytokines in multiple sclerosis
L G Filion1, G Graziani-Bowering, D Matusevicius
1Department of Biochemistry, University of Ottawa, Ottawa, Ontario, Canada. lfilion@uottowa.ca
Clinical and Experimental Immunology
|February 4, 2003
Summary
Monocytes (MO) in multiple sclerosis (MS) patients release inflammatory cytokines like IL-6, IL-12, and TNF-alpha, especially in relapsing-remitting MS without therapy and secondary progressive MS. IFN-beta therapy modulates these levels.
Area of Science:
- Immunology
- Neuroscience
- Cell Biology
Background:
- Multiple Sclerosis (MS) is an inflammatory autoimmune disease involving T cells, B cells, and monocytes (MO).
- Inflammation is prominent in relapsing-remitting MS (RRMS) but is thought to decrease in secondary progressive MS (SPMS).
Purpose of the Study:
- To compare proinflammatory and regulatory cytokine production by MO in RRMS patients with or without IFN-beta therapy, SPMS patients, and healthy controls (HC).
Main Methods:
- Monocytes (MO) were isolated using density-gradient techniques.
- Cytokine levels were assessed using RNase protection assay, ELISA, and intracellular cytokine staining.
Main Results:
- Elevated levels of IL-6, IL-12, and TNF-alpha were observed in MO from RRMS patients not receiving therapy and SPMS patients compared to HC and RRMS patients on therapy.
- These increases were consistent across all three cytokine detection methods.
Conclusions:
- Monocytes (MO) from MS patients produce both proinflammatory and regulatory cytokines, with levels influenced by IFN-beta therapy.
- Despite assumptions of diminished inflammation in SPMS, high levels of inflammatory cytokines persist, suggesting potential benefits from IFN-beta or IL-10 treatments.
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