ArticleJournal of immunology (Baltimore, Md. : 1950)2009
A single nucleotide polymorphism in Tyk2 controls susceptibility to experimental allergic encephalomyelitis.
Article in Journal of immunology (Baltimore, Md. : 1950), 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 34 citations in OpenAlex.
- Tyk2 Targeting in Immune-Mediated Inflammatory Diseases.International journal of molecular sciences · 2023Review
- Current understanding of the role of tyrosine kinase 2 signaling in immune responses.World journal of biological chemistry · 2022Review
- Novel Small Molecule Tyrosine Kinase 2 Pseudokinase Ligands Block Cytokine-Induced TYK2-Mediated Signaling Pathways.Frontiers in immunology · 2022Article
- IL-23/IL-17 Axis in Inflammatory Rheumatic Diseases.Clinical reviews in allergy & immunology · 2021Review
- Review
- Modeling month-season of birth as a risk factor in mouse models of chronic disease: from multiple sclerosis to autoimmune encephalomyelitis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2017Article
- 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
- Translational utility of experimental autoimmune encephalomyelitis: recent developments.Journal of inflammation research · 2015Review
- Inhibition of TYK2 and JAK1 ameliorates imiquimod-induced psoriasis-like dermatitis by inhibiting IL-22 and the IL-23/IL-17 axis.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Histamine H₂ receptor signaling × environment interactions determine susceptibility to experimental allergic encephalomyelitis.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2014Article
- Sex-specific control of central nervous system autoimmunity by p38 mitogen-activated protein kinase signaling in myeloid cells.Annals of neurology · 2014Article
- Forward genetic approaches for elucidation of novel regulators of Lyme arthritis severity.Frontiers in cellular and infection microbiology · 2014Review
- Impact of microbes on autoimmune diseases.Archivum immunologiae et therapiae experimentalis · 2013Review
- Establishing the role of tyrosine kinase 2 in cancer.Oncoimmunology · 2013Article
- Progress in multiple sclerosis genetics.Current genomics · 2012Article
- Enabling structure-based drug design of Tyk2 through co-crystallization with a stabilizing aminoindazole inhibitor.BMC structural biology · 2012Article
- Identification of Orch3, a locus controlling dominant resistance to autoimmune orchitis, as kinesin family member 1C.PLoS genetics · 2012Article
- Genetics of experimental allergic encephalomyelitis supports the role of T helper cells in multiple sclerosis pathogenesis.Annals of neurology · 2011Article
- Tyrosine kinases in inflammatory dermatologic disease.Journal of the American Academy of Dermatology · 2011Review
- Tyrosine kinase 2 controls IL-1ß production at the translational level.Journal of immunology (Baltimore, Md. : 1950) · 2010Article
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Genes controlling immunopathologic diseases of differing etiopathology may also influence susceptibility to autoimmune disease. B10.D1-H2(q)/SgJ mice with a 2538 G-->A missense mutation in the tyrosine kinase-2 gene (Tyk2) are susceptible to Toxoplasma gondii yet resistant to autoimmune arthritis, unlike the wild-type B10.Q/Ai substrain. To understand whether Tyk2 is also important in a second autoimmune model, experimental allergic encephalomyelitis (EAE) was induced in B10.D1-H2(q)/SgJ (Tyk2(A)) and B10.Q/Ai (Tyk2(G)) mice with the myelin oligodendrocyte glycoprotein peptide 79-96. B10.D1-H2(q)/SgJ mice were resistant to EAE whereas B10.Q/Ai mice were susceptible, and a single copy of the Tyk2(G) allele conferred EAE susceptibility in F(1) hybrids. Furthermore, EAE resistance in B10.D1-H2(q)/SgJ mice was overridden when pertussis toxin (PTX) was used to mimic the effects of environmental factors derived from infectious agents. Numerous cytokines and chemokines were increased when PTX was included in the immunization protocol. However, only RANTES, IL-6, and IFN-gamma increased significantly with both genetic compensation and PTX treatment. These data indicate that Tyk2 is a shared autoimmune disease susceptibility gene whose genetic contribution to disease susceptibility can be modified by environmental factors. Single nucleotide polymorphisms like the one that distinguishes Tyk2 alleles are of considerable significance given the potential role of gene-by-environment interactions in autoimmune disease susceptibility.
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