| IFNβ and glatiramer acetate trigger different signaling pathways to regulate the IL-1 system in multiple sclerosis. | |
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MedLine Citation:
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PMID: 21509198 Owner: NLM Status: PubMed-not-MEDLINE |
Abstract/OtherAbstract:
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Imbalance in cytokine homeostasis plays an important part in the pathogenesis of various chronic inflammatory diseases. In multiple sclerosis (MS), the pro-inflammatory cytokine interleukin-1β (IL-1β) is present in the central nervous system, being expressed mainly in infiltrating macrophages and microglial cells. IL-1β activity is inhibited by the secreted form of IL-1 receptor antagonist (sIL-1Ra) whose production is increased in patients' blood and induced in human monocytes by IFNβ and glatiramer acetate (GA)-both immunomodulators displaying similar therapeutic efficacy in MS. Because intracellular pathways are currently considered as potential therapeutic targets, identification of specific kinases used by both immunomodulators might lead to more specific therapeutic targeting. We addressed the question of intracellular pathways used by IFNβ and GA to induce sIL-1Ra in human monocytes in two recent studies. This addendum to these studies aims at discussing common pathways and different elements used by IFNβ and GA to induce sIL-1Ra in human monocytes. This pinpoints PI3Kδ activation as a requirement to induce sIL-1Ra production downstream monocyte stimulation by either IFNβ or GA. However, the immunomodulators differentially use MEK/ERK pathway to induce sIL-1Ra production in human monocytes. Together, our current studies suggest that PI3Kδ and MEK2 might represent new targets in MS therapy. |
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Authors:
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Rakel Carpintero; Danielle Burger |
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Publication Detail:
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Type: Journal Article |
Journal Detail:
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Title: Communicative & integrative biology Volume: 4 ISSN: 1942-0889 ISO Abbreviation: Commun Integr Biol Publication Date: 2011 Jan |
Date Detail:
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Created Date: 2011-04-21 Completed Date: 2011-07-14 Revised Date: 2011-07-28 |
Medline Journal Info:
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Nlm Unique ID: 101478473 Medline TA: Commun Integr Biol Country: United States |
Other Details:
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Languages: eng Pagination: 112-4 Citation Subset: - |
Affiliation:
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Division of Immunology and Allergy; Inflammation and Allergy Research Group; Hans Wilsdorf Laboratory; University Hospital and Faculty of Medicine; University of Geneva; Geneva, Switzerland. |
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