ArticleAnnals of neurology2011
Genetics of experimental allergic encephalomyelitis supports the role of T helper cells in multiple sclerosis pathogenesis.
Article in Annals of neurology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 33 citations in OpenAlex.
- Zika virus exacerbates encephalomyelitis by inducing the production of T cell-attracting chemokines in astrocytes.International immunology · 2026Article
- Astrocytic-OTUD7B ameliorates murine experimental autoimmune encephalomyelitis by stabilizing glial fibrillary acidic protein and preventing inflammation.Nature communications · 2025Article
- Analysis of CNS autoimmunity in genetically diverse mice reveals unique phenotypes and mechanisms.JCI insight · 2024Article
- Host Genetic Variation Has a Profound Impact on Immune Responses Mediating Control of Viral Load in Chronic Gammaherpesvirus Infection.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- Tolerogenic Lipid Nanoparticles for Delivering Self-Antigen mRNA for the Treatment of Experimental Autoimmune Encephalomyelitis.Pharmaceuticals (Basel, Switzerland) · 2023Article
- p38 MAP Kinase Signaling in Microglia Plays a Sex-Specific Protective Role in CNS Autoimmunity and Regulates Microglial Transcriptional States.Frontiers in immunology · 2021Article
- Identification of novel loci controlling inflammatory bowel disease susceptibility utilizing the genetic diversity of wild-derived mice.Genes and immunity · 2020Article
- Gene Expression in Spontaneous Experimental Autoimmune Encephalomyelitis Is Linked to Human Multiple Sclerosis Risk Genes.Frontiers in immunology · 2020Article
- Article
- Extracellular vesicle fibrinogen induces encephalitogenic CD8+ T cells in a mouse model of multiple sclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2019Article
- Epitope-Specific Tolerance Modes Differentially Specify Susceptibility to Proteolipid Protein-Induced Experimental Autoimmune Encephalomyelitis.Frontiers in immunology · 2017Article
- Rifampicin attenuates experimental autoimmune encephalomyelitis by inhibiting pathogenic Th17 cells responses.Journal of neurochemistry · 2016Article
- Genetic determinants of risk and progression in multiple sclerosis.Clinica chimica acta; international journal of clinical chemistry · 2015Review
- Copy number variation in Y chromosome multicopy genes is linked to a paternal parent-of-origin effect on CNS autoimmune disease in female offspring.Genome biology · 2015Article
- Genetic background effects on disease onset and lifespan of the mutant dynactin p150Glued mouse model of motor neuron disease.PloS one · 2015Article
- Article
- G proteins Gαi1/3 are critical targets for Bordetella pertussis toxin-induced vasoactive amine sensitization.Infection and immunity · 2014Article
- Selective accumulation of pro-inflammatory T cells in the intestine contributes to the resistance to autoimmune demyelinating disease.PloS one · 2014Article
- Environmental factors acting during development to influence MS risk: insights from animal studies.Multiple sclerosis (Houndmills, Basingstoke, England) · 2013Review
- The emerging role of p38 mitogen-activated protein kinase in multiple sclerosis and its models.Molecular and cellular biology · 2013Review
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Authors and funding
9 authors at 4 institutions in 1 country.
Funding
Abstract
objectiveThe major histocompatibility complex (MHC) is the primary genetic contributor to multiple sclerosis (MS) and experimental allergic encephalomyelitis (EAE), but multiple additional interacting loci are required for genetic susceptibility. The identity of most of these non-MHC genes is unknown. In this report, we identify genes within evolutionarily conserved genetic pathways leading to MS and EAE.
methodsTo identify non-MHC binary and quantitative trait loci (BTL/QTL) important in the pathogenesis of EAE, we generated phenotype-selected congenic mice using EAE-resistant B10.S and EAE-susceptible SJL mice. We hypothesized that genes linked to EAE BTL/QTL and MS-GWAS can be identified if they belong to common evolutionarily conserved pathways, which can be identified with a bioinformatic approach using Ingenuity software.
resultsMany known BTL/QTL were retained and linked to susceptibility during phenotype selection, the most significant being a region on chromosome 17 distal to H2 (Eae5). We show in pathway analysis that T helper (T(H))-cell differentiation genes are critical for both diseases. Bioinformatic analyses predicted that Eae5 is important in CD4 T-effector and/or Foxp3(+) T-regulatory cells (Tregs), and we found that B10.S-Eae5(SJL) congenic mice have significantly greater numbers of lymph node CD4 and Tregs than B10.S mice.
interpretationThese results support the polygenic model of MS/EAE, whereby MHC and multiple minor loci are required for full susceptibility, and confirm a critical genetic dependence on CD4 T(H)-cell differentiation and function in the pathogenesis of both diseases.
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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.