CLEC12A signaling represses protective immune responses and contributes to hippocampal pathology in neurotropic picornavirus infection.

ABSTRACT: 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

SUBMITTER: Ameen MK 

PROVIDER: S-EPMC12603091 | biostudies-literature | 2025 Nov

REPOSITORIES: biostudies-literature