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DOI: 10.1055/s-0041-1729428
CARD9 signaling promotes hippocampal neurogenesis and cytokine balance in a mouse model of virus-induced encephalitis
Introduction Theiler’s murine encephalomyelitis (TME) is a mouse model for virus-induced encephalitis. Innate immunity requires caspase recruitment domain family member 9 (CARD9) as a central signaling adaptor protein that functions downstream of several C-type lectin receptors including Dectin-1, Dectin-2, MCL, and Mincle. CARD9 signaling has a protective function in encephalitis caused by fungi, albeit its function in viral encephalitis remains undetermined.
Materials and methods TME virus of the DA strain was intracerebrally injected in CARD9–/– and wild type C57BL/6 mice. Brain tissues were evaluated by immunohistochemistry and RT-qPCR.
Results Immunohistochemistry showed a significant decrease of doublecortin+ neuronal progenitor cells in the dentate gyrus, while arginase 1+ M2-type macrophages/microglia were increased in CARD9–/– mice at 7- and 14-days post infection (dpi). RT-qPCR analysis revealed significantly elevated IL-1β and IFN-γ mRNA levels at 3 dpi, and an increased IL-5 mRNA expression at 7 dpi in CARD9–/– mice.
Conclusion Intact CARD9 signaling supports adult neurogenesis and cytokine balance in TMEV-induced acute encephalitis.
Publication History
Article published online:
22 June 2021
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