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Important Roles for Gamma Interferon and NKG2D in γδ T-Cell-Induced Demyelination in T-Cell Receptor β-Deficient Mice Infected with a Coronavirus
Journal article   Open access   Peer reviewed

Important Roles for Gamma Interferon and NKG2D in γδ T-Cell-Induced Demyelination in T-Cell Receptor β-Deficient Mice Infected with a Coronavirus

Ajai A Dandekar, Katherine O'Malley and Stanley Perlman
Journal of Virology, Vol.79(15), pp.9388-9396
08/2005
DOI: 10.1128/JVI.79.15.9388-9396.2005
PMCID: PMC1181615
PMID: 16014902
url
https://europepmc.org/articles/pmc1181615View
Published (Version of record) Open Access

Abstract

γδ T cells mediate demyelination in athymic (nude) mice infected with the neurotropic coronavirus mouse hepatitis virus strain JHM. Now, we show that these cells also mediate the same process in mice lacking αβ T cells (T-cell receptor β-deficient [TCRβ −/− ] mice) and demyelination is gamma interferon (IFN-γ) dependent. Most strikingly, our results also show a major role for NKG2D, expressed on γδ T cells, in the demyelinating process with in vivo blockade of NKG2D interactions resulting in a 60% reduction in demyelination. NKG2D may serve as a primary recognition receptor or as a costimulatory molecule. We show that NKG2D + γδ T cells in the JHM-infected central nervous system express the adaptor molecule DAP12 and an NKG2D isoform (NKG2D short), both required for NKG2D to serve as a primary receptor. These results are consistent with models in which γδ T cells mediate demyelination using the same effector cytokine, IFN-γ, as CD8 T cells and do so without a requirement for signaling through the TCR.
 Pathogenesis and Immunity

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