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A Single Nucleotide Polymorphism in Tyk2 Controls Susceptibility to Experimental Allergic Encephalomyelitis
Journal article   Open access   Peer reviewed

A Single Nucleotide Polymorphism in Tyk2 Controls Susceptibility to Experimental Allergic Encephalomyelitis

Karen M Spach, Rajkumar Noubade, Ben McElvany, William F Hickey, Elizabeth P Blankenhorn and Cory Teuscher
The Journal of immunology (1950), v 182(12), pp 7776-7783
15 Jun 2009
PMID: 19494301
url
https://doi.org/10.4049/jimmunol.0900142View
Published, Version of Record (VoR) Open

Abstract

EAE protein kinases neuroimmunology autoimmunity phosphatases
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 tyrosine kinase-2 ( Tyk2 ) are susceptible to Toxoplasma gondii , yet resistant to autoimmune arthritis, unlike the wild-type B10.Q/Ai substrain. To understand if 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 myelin oligodendrocyte glycoprotein peptide 79–96 . B10.D1- H2 q /SgJ ( Tyk2 A ) mice were resistant to EAE while B10.Q/Ai ( Tyk2 G ) mice were susceptible and a single copy of the Tyk2 G allele conferred EAE susceptibility in F 1 hybrids. Furthermore, EAE susceptibility in B10.D1- H2 q /SgJ ( Tyk2 A ) mice was complemented 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, interleukin-6, and interferon-γ increased significantly with both genetic compensation and PTX complementation. These data indicate that Tyk2 is a shared autoimmune disease susceptibility gene that can be complemented both genetically and environmentally. 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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Collaboration types
Domestic collaboration
Web of Science research areas
Immunology
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