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000305739 1001_ $$aAmeen, M. K.$$b0
000305739 245__ $$aCLEC12A signaling represses protective immune responses and contributes to hippocampal pathology in neurotropic picornavirus infection.
000305739 260__ $$a[London]$$bSpringer Nature$$c2025
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000305739 520__ $$aNeurotropic viruses infect the central nervous system (CNS) and can cause severe neurological disorders. Theiler's murine encephalomyelitis virus (TMEV) infection in C57BL/6 mice serves as a model for virus-induced encephalitis and hippocampal damage. C-type lectin domain family 12 member A (CLEC12A) is an inhibitory receptor, which modulates immune responses during inflammatory processes. However, the role of CLEC12A during neurotropic virus infections remains unclear. In this study, CLEC12A-deficient (CLEC12A-/-) and wild type C57BL/6 mice were infected with TMEV. Neuroinflammatory responses, viral load, and immune cell infiltration were analyzed using immunohistochemistry, RT-qPCR, and flow cytometry. CLEC12A-/- mice exhibited increased T cell sequestration in the brain, along with a higher expression of pro-inflammatory cytokine (TNF-α, IL-1β) and antigen presentation genes (CD11c, CD80, MHC-I) during acute infection. This led to an improved viral clearance in the hippocampus. CLEC12A deficiency also activates splenic CD4+ T cells and CD8+ cytotoxic T cells upon infection. Despite increased peripheral T cell activation and neuroinflammation, CLEC12A-/- mice displayed less hippocampal damage with improved neuronal and axonal integrity. In conclusion, CLEC12A signaling in C57BL/6 mice contributes to suppressive immune modulation, delaying viral elimination and exacerbating brain damage during acute neurotropic virus infection.
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000305739 650_7 $$2Other$$aAntiviral immunity
000305739 650_7 $$2Other$$aC-type lectin receptor
000305739 650_7 $$2Other$$aCLEC12A
000305739 650_7 $$2Other$$aHippocampal pathology
000305739 650_7 $$2Other$$aNeuroinflammation
000305739 650_7 $$2Other$$aTMEV
000305739 7001_ $$aStoff, M.$$b1
000305739 7001_ $$aPavasutthipaisit, S.$$b2
000305739 7001_ $$aEbbecke, T.$$b3
000305739 7001_ $$aCiurkiewicz, M.$$b4
000305739 7001_ $$aStörk, T.$$b5
000305739 7001_ $$0P:(DE-HGF)0$$aRuland, J.$$b6
000305739 7001_ $$aLepenies, B.$$b7
000305739 7001_ $$aBeineke, A.$$b8
000305739 773__ $$0PERI:(DE-600)2615211-3$$a10.1038/s41598-025-27365-3$$gVol. 15, no. 1, p. 39354$$n1$$p39354$$tScientific reports$$v15$$x2045-2322$$y2025
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