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CARD9 signaling enhances antiviral immunity in a mouse model for neurotropic virus infection
Introduction Theiler’s murine encephalomyelitis virus (TMEV) infection of C57BL/6 mice is a model for hippocampal damage and neurotropic virus infection. Caspase recruitment domain family member 9 (CARD9) is a central signaling adaptor protein that operates downstream of some C-type lectin receptors and plays an important role in innate immunity. CARD9 deficiency has been shown to enhance fungal neuroinfection. However, the effect of CARD9 signaling in viral encephalitis remains unclear.
Materials and methods CARD9–/– and wild type C57BL/6 mice were intracerebral injected with TMEV DA. Spleen tissue was analyzed by flow cytometry and brain tissue was evaluated by immunohistochemistry.
Results Flow cytometry showed an increase of activated CD4+ and CD8+ T cells in CARD9–/– mice at 14 dpi. In the hippocampus an increased number of TMEV+ cells in CARD9–/– mice was found at 7 dpi, associated with increased brain infiltrations of CD3+ T cells and CD45R+ B cells.
Conclusion CARD9 deficiency causes an impaired antiviral immunity following TMEV infection, which leads to enhanced neuroinflammation. This data support the view of a protective function of intact CARD9 signaling in acute neurotropic virus infection.
08 July 2020 (online)
© Georg Thieme Verlag KG
Stuttgart · New York