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DOI: 10.1055/s-0039-1688640
Neuroprotective function of CARD9 signaling in acute Theiler's murine encephalomyelitis infection
Publication History
Publication Date:
18 June 2019 (online)
Introduction:
Theiler's murine encephalomyelitis virus (TMEV) infection of wild type (C57BL/6) mice represents an animal model for hippocampal degeneration and epilepsy. Caspase recruitment domain family member 9 (CARD9) is a signaling protein which plays a role in inflammation and immunity. So far, the effect of CARD9 signaling in viral encephalitis remains undetermined.
Materials and methods:
CARD9-/- and C57BL/6 (wild type control) mice were intracerebrally inoculated with TMEV. Brain tissue was investigated by histology and immunohistochemistry. Spleen tissue was analyzed by flow cytometry.
Results:
Results showed an enhanced brain inflammation at 7 dpi in CARD9-/- mice compared to wild type mice. In addition, the number of beta-amyloid precursor protein-positive axons was significantly increased in the hippocampus of CARD9-/- mice at 7 and 14 dpi. T cell activation was significantly increased in CD4+ and CD8+ T cells in CARD9-/- mice at 14 dpi as indicated by CD62L down-regulation.
Conclusion:
CARD9 deficiency causes axonal damage in seizure-prone C57BL/6 mice following TMEV infection, indicating a neuroprotective function of intact CARD9 signaling in acute viral infection.
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