ReviewJournal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology2010
Studies in the modulation of experimental autoimmune encephalomyelitis.
Review in Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
9 citing papers in PubMed, 14 citations in OpenAlex.
- Curdlan, a Microbial β-Glucan, Has Contrasting Effects on Autoimmune and Viral Models of Multiple Sclerosis.Frontiers in cellular and infection microbiology · 2022Article
- Bioinformatics Analyses Determined the Distinct CNS and Peripheral Surrogate Biomarker Candidates Between Two Mouse Models for Progressive Multiple Sclerosis.Frontiers in immunology · 2019Article
- Acthar gel treatment suppresses acute exacerbations in a murine model of relapsing-remitting multiple sclerosis.Autoimmunity · 2015Article
- DA virus mutant H101 has altered CNS pathogenesis and causes immunosuppression.Journal of neuroimmunology · 2014Article
- Targeting insulin-like growth factor 1 leads to amelioration of inflammatory demyelinating disease.PloS one · 2014Article
- Possible role of interleukin-17 in a prime/challenge model of multiple sclerosis.Journal of neurovirology · 2012Article
- Two discreet subsets of CD8 T cells modulate PLP(91-110) induced experimental autoimmune encephalomyelitis in HLA-DR3 transgenic mice.Journal of autoimmunity · 2012Article
- Immunomodulation of experimental allergic encephalomyelitis by cinnamon metabolite sodium benzoate.Immunopharmacology and immunotoxicology · 2011Article
- Neuroimmune pharmacological control of EAE.Journal of neuroimmune pharmacology : the official journal of the Society on NeuroImmune Pharmacology · 2010Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Experimental autoimmune encephalomyelitis (EAE), an experimental model for multiple sclerosis, can be induced through inoculation with several different central nervous system (CNS) proteins or peptides. Modulation of EAE, resulting in either protection from EAE or enhancement of EAE, can also be accomplished through either vaccination or DNA immunization with molecular mimics of self-CNS proteins. Previously published data on this method of EAE modulation will be reviewed. New data is presented, which demonstrates that EAE can also be modulated through the administration of the beta-(1,3)-D-glucan, curdlan. Dendritic cells stimulated by curdlan are involved in the differentiation of the interleukin-17 producing subset of CD4(+) T cells that are recognized effector cells in EAE. Using two different systems to study the effects of curdlan on EAE, it was found that curdlan increased the incidence of EAE and/or the severity of the disease course.
Indexed as
Identifiers
What OpenQuestion holds
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.