ArticleBrain, behavior, and immunity2025
Microglia-specific Ido2 deficiency attenuates ictogenesis in the TMEV model of viral encephalitis.
Article in Brain, behavior, and immunity, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- Microglia and neuroinflammation: An in-depth analysis from functional diversity to disease mechanisms.Clinical and translational medicine · 2026Review
- Pathogens of the human central nervous system-the major viral pathogens.Journal of neurovirology · 2026Review
- The kynurenine pathway storm in epilepsy: mechanisms and therapeutic implications.Acta epileptologica · 2026Review
- Maternal Inflammation Alters Nuclear and Mitochondrial DNA Methylation Patterns in Neonatal Brain Monocytes.Cells · 2026Article
- IDO family: the metabolic crossroads connecting immunity, nerves and tumors.Journal of translational medicine · 2026Review
- Glial-mediated immune modulation in glaucomatous neurodegeneration: mechanisms and therapeutic implications.Frontiers in immunology · 2025Review
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Authors and funding
6 authors.
Funding
Abstract
Viral encephalitis is a serious condition that causes acute neuroinflammation, neurodegeneration, cognitive deficits and behavioral changes, while putting patients at risk of developing seizures (ictogenesis) and post-encephalitis epilepsy. Intracerebral injection of C57BL/6 mice with Theiler's murine encephalomyelitis virus (TMEV) is a model of viral encephalitis that causes behavioral seizures along with substantial neurodegeneration and neuroinflammation. This model is considered a benchmark preclinical paradigm for the investigation of hippocampal-dependent viral ictogenesis and temporal lobe epilepsy. Inflammation-induced indolealine2,3-deoxygenase (Ido) 1 and 2 initiate the conversion of tryptophan into kynurenine, which is subsequently converted into downstream neuroactive metabolites with the ability to modify behavioral seizures. Ido1 and Ido2 have also been shown to have non-redundant roles in modulating several inflammatory diseases. We have previously shown that Ido1 deficiency increases TMEV-induced behavioral seizure incidence using wild type (WT, C57BL/6J) mice. Here, we extend those findings to Ido2 deficiencies. We find that Ido2
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