ArticleThe American journal of pathology2000
Identification of genetic loci controlling the characteristics and severity of brain and spinal cord lesions in experimental allergic encephalomyelitis.
Article in The American journal of pathology, 2000. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers, 1 of them a synthesis that pooled it.
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Who cites it
42 citing papers in PubMed, 1 synthesis or guideline pooled it, 106 citations in OpenAlex.
- Multiparametric and semiquantitative scoring systems for the evaluation of mouse model histopathology--a systematic review.BMC veterinary research · 2013Pooled it
- Role of Caveolin-1 in Inflammation: Genetic Predisposition and Potential Implication for Multiple Sclerosis.Genes · 2026Review
- Case report: HLA-B35-associated optic neuritis.Frontiers in ophthalmology · 2024Article
- Biological Sex As a Critical Variable in CD4Antioxidants & redox signaling · 2022Review
- Armc5 deletion causes developmental defects and compromises T-cell immune responses.Nature communications · 2017Article
- Genetic determinants of risk and progression in multiple sclerosis.Clinica chimica acta; international journal of clinical chemistry · 2015Review
- Exacerbation of autoimmune neuroinflammation by dietary sodium is genetically controlled and sex specific.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2015Article
- Article
- Identification of Orch3, a locus controlling dominant resistance to autoimmune orchitis, as kinesin family member 1C.PLoS genetics · 2012Article
- Genome-wide association study of severity in multiple sclerosis.Genes and immunity · 2011Article
- 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
- Genetic correlations of brain lesion distribution in multiple sclerosis: an exploratory study.AJNR. American journal of neuroradiology · 2011Article
- Multiple linked quantitative trait loci within the Tmevd2/Eae3 interval control the severity of experimental allergic encephalomyelitis in DBA/2J mice.Genes and immunity · 2010Article
- Identification of a novel cerebral malaria susceptibility locus (Berr5) on mouse chromosome 19.Genes and immunity · 2010Article
- Substrain differences reveal novel disease-modifying gene candidates that alter the clinical course of a rodent model of multiple sclerosis.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
- The postnatal maternal environment affects autoimmune disease susceptibility in A/J mice.Cellular immunology · 2010Article
- A single nucleotide polymorphism in Tyk2 controls susceptibility to experimental allergic encephalomyelitis.Journal of immunology (Baltimore, Md. : 1950) · 2009Article
- Fine mapping of gene regions regulating neurodegeneration.PloS one · 2009Article
- IL-13-mediated gender difference in susceptibility to autoimmune encephalomyelitis.Journal of immunology (Baltimore, Md. : 1950) · 2008Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Experimental allergic encephalomyelitis (EAE) is the principal genetically determined animal model for multiple sclerosis (MS), the major inflammatory disease of the central nervous system (CNS). Although genetics clearly play a role in susceptibility to MS, attempts to identify the underlying genes have been disappointing. Considerable variation exists between MS patients with regard to the severity of clinical signs, mechanism of demyelination, and location of CNS lesions, confounding the interpretation of genetic data. A mouse-human synteny mapping approach may allow the identification of candidate susceptibility loci for MS based on the location of EAE susceptibility loci. To date, 16 regions of the mouse genome have been identified that control susceptibility or clinical signs of EAE. In this work, we examined the genetic control of histopathological lesions of EAE in an F2 intercross population generated from the EAE susceptible SJL/J and EAE resistant B10.S/DvTe mouse strains. Composite interval mapping was used to identify 10 quantitative trait loci (QTL), including seven newly identified loci controlling the distribution and severity of CNS lesions associated with murine EAE. QTL on chromosome 10 control lesions in the brain, whereas QTL on chromosomes 3, 7, and 12 control lesions in the spinal cord. Furthermore, sexually dimorphic QTL on chromosomes 2, 9, and 11 control CNS lesions in females, whereas QTL on chromosomes 10, 11, 12, 16, and 19 control lesions in males. Our results suggest that the severity and location of CNS lesions in EAE are genetically controlled, and that the genetic component controlling the character and severity of the lesions can be influenced by sex.
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