ArticleGenes and immunity2010
Multiple loci comprising immune-related genes regulate experimental neuroinflammation.
Article in Genes and immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 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
12 citing papers in PubMed, 26 citations in OpenAlex.
- Hunting for Genes Underlying Emotionality in the Laboratory Rat: Maps, Tools and Traps.Current neuropharmacology · 2023Review
- Multiple sclerosis risk loci and disease severity in 7,125 individuals from 10 studies.Neurology. Genetics · 2016Article
- Complement receptor 2 is up regulated in the spinal cord following nerve root injury and modulates the spinal cord response.Journal of neuroinflammation · 2015Article
- Genetic determinants of risk and progression in multiple sclerosis.Clinica chimica acta; international journal of clinical chemistry · 2015Review
- Fine-mapping QTLs in advanced intercross lines and other outbred populations.Mammalian genome : official journal of the International Mammalian Genome Society · 2014Review
- Identification of candidate risk gene variations by whole-genome sequence analysis of four rat strains commonly used in inflammation research.BMC genomics · 2014Article
- Combining genetic mapping with genome-wide expression in experimental autoimmune encephalomyelitis highlights a gene network enriched for T cell functions and candidate genes regulating autoimmunity.Human molecular genetics · 2013Article
- Anti-MOG antibodies are under polygenic regulation with the most significant control coming from the C-type lectin-like gene locus.Genes and immunity · 2013Article
- Article
- The calcitonin receptor gene is a candidate for regulation of susceptibility to herpes simplex type 1 neuronal infection leading to encephalitis in rat.PLoS pathogens · 2012Article
- Strain-dependent variation in the early transcriptional response to CNS injury using a cortical explant system.Journal of neuroinflammation · 2011Article
- Fine-mapping resolves Eae23 into two QTLs and implicates ZEB1 as a candidate gene regulating experimental neuroinflammation in rat.PloS one · 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
8 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
A 58 Mb region on rat chromosome 4 known to regulate experimental autoimmune encephalomyelitis (EAE) was genetically dissected. High-resolution linkage analysis in an advanced intercross line (AIL) revealed four quantitative trait loci (QTLs), Eae24-Eae27. Both Eae24 and Eae25 regulated susceptibility and severity phenotypes, whereas Eae26 regulated severity and Eae27 regulated susceptibility. Analyses of the humoral immune response revealed that the levels of serum anti-myelin oligodendrocyte glycoprotein (MOG) immunoglobin G1 (IgG1) antibodies are linked to Eae24 and anti-MOG IgG2b antibodies are linked to both Eae24 and Eae26. We tested the parental DA strain and six recombinant congenic strains that include overlapping fragments of this region in MOG-EAE. Eae24 and Eae25 showed significant protection during the acute phase of EAE, whereas Eae25 and Eae26 significantly modified severity but not susceptibility. The smallest congenic fragment, which carries Eae25 alone, influenced both susceptibility and severity, and protected from the chronic phase of disease. These results support the multiple QTLs identified in the AIL. By demonstrating several QTLs comprising immune-related genes, which potentially interact, we provide a significant step toward elucidation of the polygenically regulated pathogenesis of MOG-EAE and possibly multiple sclerosis (MS), and opportunities for comparative genetics and testing in MS case-control cohorts.
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.