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Coronavirus-induced demyelination occurs in the absence of CD28 costimulatory signals
Infection of mice with mouse hepatitis virus (MHV) strain A59 results in acute encephalitis, hepatitis, and chronic demyelinating disease. T lymphocytes play an important role in MHV infection, and costimulatory signals are an important component of T cell function. To elucidate the role of the main...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Elsevier/North-Holland
2004
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7119462/ https://www.ncbi.nlm.nih.gov/pubmed/14698856 http://dx.doi.org/10.1016/j.jneuroim.2003.10.053 |
Sumario: | Infection of mice with mouse hepatitis virus (MHV) strain A59 results in acute encephalitis, hepatitis, and chronic demyelinating disease. T lymphocytes play an important role in MHV infection, and costimulatory signals are an important component of T cell function. To elucidate the role of the main costimulatory molecule, CD28, in MHV pathogenesis and demyelination, we examined the kinetics of MHV-A59 infection in CD28 knockout mice. MHV-A59-infected CD28 knockout mice developed acute encephalitis and hepatitis, and the same degree of chronic demyelination as normal C57Bl/6 (B6) mice. Thus, CD28, the costimulatory T cell molecule, is not required for MHV infection and MHV-induced demyelination. |
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