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Mouse hepatitis virus pathogenesis in the central nervous system is independent of IL-15 and natural killer cells

Infection by the neurotropic JHM strain of mouse hepatitis virus (JHMV) results in an acute encephalomyelitis associated with demyelination. T cells are critical in controlling viral replication, but also contribute to central nervous system (CNS) pathogenesis. To reveal a role for innate effectors...

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Detalles Bibliográficos
Autores principales: Zuo, Jun, Stohlman, Stephen A., Hoskin, Jason B., Hinton, David R., Atkinson, Roscoe, Bergmann, Cornelia C.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Elsevier Inc. 2006
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7111870/
https://www.ncbi.nlm.nih.gov/pubmed/16510164
http://dx.doi.org/10.1016/j.virol.2006.01.027
Descripción
Sumario:Infection by the neurotropic JHM strain of mouse hepatitis virus (JHMV) results in an acute encephalomyelitis associated with demyelination. T cells are critical in controlling viral replication, but also contribute to central nervous system (CNS) pathogenesis. To reveal a role for innate effectors in anti-viral immunity and neurological disease, JHMV pathogenesis was studied in mice deficient in interleukin-15 (IL-15(−/−)) and natural killer (NK) cells. Clinical disease, CNS inflammation and demyelination in infected IL-15(−/−) mice were similar to wild-type mice. Despite the absence of NK cells and suboptimal CD8(+) T cell responses, IL-15(−/−) mice controlled JHMV replication as efficiently as wild-type mice. Similar kinetics of class I and class II upregulation on microglia further suggested no role of NK cells in regulating major histocompatibility complex (MHC) molecule expression on resident CNS cells. IL-15 and NK cells thus appear dispensable for anti-viral immunity and CNS pathogenesis during acute JHMV infection.