ArticleFrontiers in immunology2021
Fas/FasL Contributes to HSV-1 Brain Infection and Neuroinflammation.
Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 31 citations in OpenAlex.
- Inflammation increases the penetrance of behavioral impairment in Shank3 haploinsufficiency mice - can it explain the behavioral regression in Autism?Molecular psychiatry · 2026Article
- Eupatorium perfoliatum Counteracts TNF-α Mediated Pathogenesis in Chikungunya Virus Infection.Applied biochemistry and biotechnology · 2026Article
- The Mediating Factor of Immune Cell in the Causal Relationship Between Cardiovascular Disease-Related Plasma Proteins and Parkinson's Disease: A Network Mendelian Randomization Analysis.Mediators of inflammation · 2026Article
- Article
- An immunocompetent mouse model revealed that congenital Zika virus infection disrupted hippocampal function by activating autophagy.Emerging microbes & infections · 2025Article
- Inflammation increases the penetrance of behavioral impairment inbioRxiv : the preprint server for biology · 2025Article
- HSV-1 hijacks mitochondrial dynamics: potential molecular mechanisms linking viral infection to neurodegenerative disorders.Apoptosis : an international journal on programmed cell death · 2025Review
- The Role of Nitric Oxide in HSV-1 Infection: The Use of an Inducible Nitric Synthase Inhibitor Aminoguanidine to Treat Neuroinflammation.Microorganisms · 2025Article
- Polymorphisms Influence the Expression of the Fas and FasL Genes in COVID-19.International journal of molecular sciences · 2025Article
- The Influence of the AgNPs Ligand on the Antiviral Activity Against HSV-2.International journal of nanomedicine · 2025Article
- FAS mediates apoptosis, inflammation, and treatment of pathogen infection.Frontiers in cellular and infection microbiology · 2025Review
- Helminthic larval stage induces cellular apoptosis via caspase 9-mediated mitochondrial dysfunction.Frontiers in immunology · 2025Article
- miRNA-431-5p enriched in EVs derived from IFN-β stimulated MSCs potently inhibited ZIKV through CD95 downregulation.Stem cell research & therapy · 2024Article
- Fas/FasL-Mediated Apoptosis and Inflammation Contribute to Recovery from HSV-2-Mediated Spinal Cord Infection.Viruses · 2024Article
- Fas ligand regulate nerve injury and repair by affecting AKT, β-catenin, and NF-κB pathways.IBRO neuroscience reports · 2024Article
- Identification of FasL as a crucial host factor driving COVID-19 pathology and lethality.Cell death and differentiation · 2024Article
- Nicotine suppresses crystalline silica-induced astrocyte activation and neuronal death by inhibiting NF-κB in the mouse hippocampus.CNS neuroscience & therapeutics · 2024Article
- Die Hard: Necroptosis and its Impact on Age-Dependent Neuroinflammatory Diseases.Frontiers in cell death · 2024Article
- FAS-mediated circRNA-miRNA-mRNA Crosstalk Network Regulates Immune Cell Infiltration in Cerebral Infarction.Journal of molecular neuroscience : MN · 2023Article
- Apoptosis and Phagocytosis as Antiviral Mechanisms.Sub-cellular biochemistry · 2023Article
Corrections and comments
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Authors and funding
5 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The Fas/FasL pathway plays a key role in immune homeostasis and immune surveillance. In the central nervous system (CNS) Fas/FasL is involved in axonal outgrowth and adult neurogenesis. However, little is known about the role of the Fas/FasL pathway in herpes encephalitis. In this study, we used a neuropathogenic clinical strain of herpes simplex virus type 1 (HSV-1) to explore infection-induced inflammation and immune responses in the mouse brain and the role of Fas/FasL in antiviral CNS immunity. HSV-1 CNS infection induced the infiltration of Fas- FasL-bearing monocytes and T cells in the brain and also to an up-regulation of Fas and FasL expression on resident astrocytes and microglia within infected sites. Upon infection, Fas- and FasL-deficient mice (lpr and gld) were partially protected from encephalitis with a decreased morbidity and mortality compared to WT mice. Fas/FasL deficiency promoted cell-mediated immunity within the CNS. Fas receptor stimulation abrogated HSV-1 induced activation and inflammatory reactions in microglia from WT mice, while lack of Fas or FasL led to a more pronounced activation of monocytes and microglia and also to an enhanced differentiation of these cells into a pro-inflammatory M1 phenotype. Furthermore, the specific immune system was more efficient in Fas- and FasL-deficient mice with significantly higher numbers of infiltrating HSV-1-specific cytotoxic T cells in the brain. Our data indicate that the Fas/FasL pathway leads to excessive neuroinflammation during HSV-1 infection, which is associated with a diminished anti-viral response and an excessive neuroinflammation.
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