ArticleJournal of neuroimmunology2013
Glatiramer acetate biases dendritic cells towards an anti-inflammatory phenotype by modulating OPN, IL-17, and RORγt responses and by increasing IL-10 production in experimental allergic encephalomyelitis.
Article in Journal of neuroimmunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 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.
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Who cites it
10 citing papers in PubMed, 22 citations in OpenAlex.
- Inflammation and Elevated Osteopontin in Plasma and CSF in Cerebral Malaria Compared toInternational journal of molecular sciences · 2024Article
- Targeting Neuroinflammation to Alleviate Chronic Olfactory Dysfunction in Long COVID: A Role for Investigating Disease-Modifying Therapy (DMT)?Life (Basel, Switzerland) · 2023Article
- TheNeural regeneration research · 2021Review
- To the Brain and Back: Migratory Paths of Dendritic Cells in Multiple Sclerosis.Journal of neuropathology and experimental neurology · 2018Review
- Dendritic cells as therapeutic targets in neuroinflammation.Cellular and molecular life sciences : CMLS · 2016Review
- Protective Microglia and Their Regulation in Parkinson's Disease.Frontiers in molecular neuroscience · 2016Review
- M1 and M2 immune activation in Parkinson's Disease: Foe and ally?Neuroscience · 2015Review
- Seeking balance: Potentiation and inhibition of multiple sclerosis autoimmune responses by IL-6 and IL-10.Cytokine · 2015Review
- Role of the immunogenic and tolerogenic subsets of dendritic cells in multiple sclerosis.Mediators of inflammation · 2015Review
- Restoration of axon conduction and motor deficits by therapeutic treatment with glatiramer acetate.Journal of neuroscience research · 2014Article
Corrections and comments
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Authors and funding
8 authors at 1 institution in 1 country.
Funding
Abstract
Paralleling our previous mechanistic studies of glatiramer acetate (GA; Copaxone) activity, we show that GA curbs the expression of Toll-like receptor (TLR) 9 and the universal adapter protein Myd88 in mice with EAE, the animal model for multiple sclerosis. Concurrent with enhanced dendritic cell (DC) production of IL-10, GA interferes with OPN, IL-17, and ROR gamma expression in DCs of mice with EAE, and suppresses brain expression of the EAE-induced chemokines, MIP1α and β, IP-10 and RANTES. Thus GA not only biases dendritic cells towards an anti-inflammatory phenotype, but also suppresses the expression of factors that affect the blood-brain barrier penetration during neuroinflammation.
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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.