ArticleCommunicative & integrative biology2011
IFNβ and glatiramer acetate trigger different signaling pathways to regulate the IL-1 system in multiple sclerosis.
Article in Communicative & integrative biology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
5 citing papers in PubMed, 9 citations in OpenAlex.
- Trial
- Influence of Genetic Polymorphisms on Clinical Outcomes of Glatiramer Acetate in Multiple Sclerosis Patients.Journal of personalized medicine · 2021Review
- New Insights into the Role of IL-1β in Experimental Autoimmune Encephalomyelitis and Multiple Sclerosis.Journal of immunology (Baltimore, Md. : 1950) · 2017Review
- Myeloid cell transmigration across the CNS vasculature triggers IL-1β-driven neuroinflammation during autoimmune encephalomyelitis in mice.The Journal of experimental medicine · 2016Article
- Association of missense mutations of Mediterranean fever (MEFV) gene with multiple sclerosis in Turkish population.Journal of molecular neuroscience : MN · 2013Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.