ArticleGenetics2006
eae36, a locus on mouse chromosome 4, controls susceptibility to experimental allergic encephalomyelitis in older mice and mice immunized in the winter.
Article in Genetics, 2006. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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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
13 citing papers in PubMed, 24 citations in OpenAlex.
- Seasonal Variations in Macrophages/Microglia Underlie Changes in the Mouse Model of Multiple Sclerosis Severity.Molecular neurobiology · 2020Article
- Minor genomic differences between related B6 and B10 mice affect severity of schistosome infection by governing the mode of dendritic cell activation.European journal of immunology · 2015Article
- Environmental factors acting during development to influence MS risk: insights from animal studies.Multiple sclerosis (Houndmills, Basingstoke, England) · 2013Review
- Induction and regulation of pathogenic Th17 cell responses in schistosomiasis.Seminars in immunopathology · 2012Review
- Genetics of experimental allergic encephalomyelitis supports the role of T helper cells in multiple sclerosis pathogenesis.Annals of neurology · 2011Article
- Strain-dependent variation in the early transcriptional response to CNS injury using a cortical explant system.Journal of neuroinflammation · 2011Article
- Animal models of multiple sclerosis--potentials and limitations.Progress in neurobiology · 2010Review
- Fine-mapping resolves Eae23 into two QTLs and implicates ZEB1 as a candidate gene regulating experimental neuroinflammation in rat.PloS one · 2010Article
- The postnatal maternal environment affects autoimmune disease susceptibility in A/J mice.Cellular immunology · 2010Article
- Genetic control of severe egg-induced immunopathology and IL-17 production in murine schistosomiasis.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Enhancing the ability of experimental autoimmune encephalomyelitis to serve as a more rigorous model of multiple sclerosis through refinement of the experimental design.Comparative medicine · 2009Article
- Cutting edge: the Y chromosome controls the age-dependent experimental allergic encephalomyelitis sexual dimorphism in SJL/J mice.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- An engineered monomer of CCL2 has anti-inflammatory properties emphasizing the importance of oligomerization for chemokine activity in vivo.Journal of leukocyte biology · 2008Article
Corrections and comments
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Authors and funding
4 authors at 4 institutions in 1 country.
Funding
Abstract
Genetic factors are believed to contribute to multiple sclerosis (MS) susceptibility; however, strong evidence implicating intrinsic and environmental factors in the etiopathogenesis of MS also exists. Susceptibility to experimental allergic encephalomyelitis (EAE), the principal animal model of MS, is also influenced by nongenetic factors, including age and season at immunization. This suggests that age- and season-by-gene interactions exist and that different susceptibility loci may influence disease as a function of the two parameters. In this study, linkage analysis based on genome exclusion mapping was carried out using age and season at immunization restricted cohorts of (B10.S x SJL/J) F2 intercross mice in an effort to identify such linkages. Significant linkage of EAE to eae4 and eae5 was detected with 6- to 12-week-old and summer cohorts. In contrast, significant linkage of EAE to eae4 and eae5 was not detected with the >12-week-old and winter/spring populations. Rather, significant linkage to D4Mit203 at 128.50 Mb on chromosome 4 was detected with animals that were >12 weeks old at the time of immunization or were immunized in the winter. This previously unidentified locus has been designated eae36. These results support the existence of age- and season-by-gene-specific interactions in the genetic control of susceptibility to autoimmune inflammatory disease of the central nervous system and suggest that late-onset MS may be immunogenetically distinct.
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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.