Home > Publications database > CLEC12A signaling represses protective immune responses and contributes to hippocampal pathology in neurotropic picornavirus infection. > print

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082 _ _ |a 600
100 1 _ |a Ameen, M. K.
|b 0
245 _ _ |a CLEC12A signaling represses protective immune responses and contributes to hippocampal pathology in neurotropic picornavirus infection.
260 _ _ |a [London]
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|b Springer Nature
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520 _ _ |a Neurotropic viruses infect the central nervous system (CNS) and can cause severe neurological disorders. Theiler's murine encephalomyelitis virus (TMEV) infection in C57BL/6 mice serves as a model for virus-induced encephalitis and hippocampal damage. C-type lectin domain family 12 member A (CLEC12A) is an inhibitory receptor, which modulates immune responses during inflammatory processes. However, the role of CLEC12A during neurotropic virus infections remains unclear. In this study, CLEC12A-deficient (CLEC12A-/-) and wild type C57BL/6 mice were infected with TMEV. Neuroinflammatory responses, viral load, and immune cell infiltration were analyzed using immunohistochemistry, RT-qPCR, and flow cytometry. CLEC12A-/- mice exhibited increased T cell sequestration in the brain, along with a higher expression of pro-inflammatory cytokine (TNF-α, IL-1β) and antigen presentation genes (CD11c, CD80, MHC-I) during acute infection. This led to an improved viral clearance in the hippocampus. CLEC12A deficiency also activates splenic CD4+ T cells and CD8+ cytotoxic T cells upon infection. Despite increased peripheral T cell activation and neuroinflammation, CLEC12A-/- mice displayed less hippocampal damage with improved neuronal and axonal integrity. In conclusion, CLEC12A signaling in C57BL/6 mice contributes to suppressive immune modulation, delaying viral elimination and exacerbating brain damage during acute neurotropic virus infection.
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650 _ 7 |a Antiviral immunity
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650 _ 7 |a C-type lectin receptor
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650 _ 7 |a CLEC12A
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650 _ 7 |a Hippocampal pathology
|2 Other
650 _ 7 |a Neuroinflammation
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650 _ 7 |a TMEV
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700 1 _ |a Stoff, M.
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700 1 _ |a Pavasutthipaisit, S.
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700 1 _ |a Ebbecke, T.
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700 1 _ |a Ciurkiewicz, M.
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700 1 _ |a Störk, T.
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700 1 _ |a Ruland, J.
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700 1 _ |a Lepenies, B.
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700 1 _ |a Beineke, A.
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773 _ _ |a 10.1038/s41598-025-27365-3
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910 1 _ |a Deutsches Krebsforschungszentrum
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