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Interferon-beta not only inhibits interleukin-1α and tumor necrosis factor-α but stimulates interleukin-1 receptor antagonist production in human peripheral blood mononuclear cells |
European Cytokine Network. Volume 8, Number 4, 345-9, December 1997, Review
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 Summary
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Author(s) : Joëlle Coclet-Ninin, Jean-Michel Dayer and Danielle Burger, Division of Immunology and Allergy, Clinical Immunology Unit (Hans Wilsdorf Laboratory), Department of Internal Medicine, University Hospital, Geneva, Switzerland. |
Summary : Imbalance between pro-inflammatory cytokines such as interleukin-1 (IL-1) and tumor necrosis factor-α (TNF-α) and their respective inhibitors is likely to be involved in the pathogenesis of chronic inflammatory disorders such as multiple sclerosis and rheumatoid arthritis. Increasing evidence suggests that the administration of interferon-β (IFN-β) displays some efficacy in the treatment of patients with relapsing-remitting multiple sclerosis. The aim of the present study was to determine the effect of IFN-β on the production of pro-inflammatory cytokines and their inhibitors by stimulated peripheral blood mononuclear cells (PBMC). IFN-β decreased the production of both IL-1β and TNF-α in a dose-dependent manner, by up to 80% and 55%, respectively. Simultaneously, IFN-β increased the production of IL-1 receptor antagonist (IL-1Ra) by 37% and did not modulate the release of TNF-soluble receptors (TNF-sRs) p55 and p75. Therefore, by favoring the production of cytokine antagonists over that of pro-inflammatory cytokines, IFN-β induces an imbalance supporting anti-inflammatory processes. This effect might account for some of the therapeutic benefit of IFN-β. |
Keywords : interferon-β, interleukin-β1, tumor necrosis factor-α, interleukin-1 receptor antagonist, TNF soluble receptors, inflammation. |
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