ArticleJournal of immunology (Baltimore, Md. : 1950)2012
Mice with mutations in Fas and Fas ligand demonstrate increased herpetic stromal keratitis following corneal infection with HSV-1.
Article in Journal of immunology (Baltimore, Md. : 1950), 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 20 papers.
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Who cites it
20 citing papers in PubMed, 24 citations in OpenAlex.
- Article
- FAS mediates apoptosis, inflammation, and treatment of pathogen infection.Frontiers in cellular and infection microbiology · 2025Review
- Infectious Keratitis in Patients Over 65: A Review on Treatment and Preserving Eyesight.Clinical interventions in aging · 2024Review
- Living with your biome: how the bacterial microbiome impacts ocular surface health and disease.Expert review of ophthalmology · 2024Article
- Sensory Nerve Retraction and Sympathetic Nerve Innervation Contribute to Immunopathology of Murine Recurrent Herpes Stromal Keratitis.Investigative ophthalmology & visual science · 2022Article
- Pigment Epithelium-derived Factor secreted by corneal epithelial cells regulates dendritic cell maturation in dry eye disease.The ocular surface · 2020Article
- CD28 Costimulation Is Required for Development of Herpetic Stromal Keratitis but Does Not Prevent Establishment of Latency.Journal of virology · 2019Article
- Pathological processes activated by herpes simplex virus-1 (HSV-1) infection in the cornea.Cellular and molecular life sciences : CMLS · 2019Review
- The immunoregulatory role of corneal epithelium-derived thrombospondin-1 in dry eye disease.The ocular surface · 2018Article
- When Clarity Is Crucial: Regulating Ocular Surface Immunity.Trends in immunology · 2018Review
- Inhibition of HUVEC tube formation via suppression of NFκB suggests an anti-angiogenic role for SLURP1 in the transparent cornea.Experimental eye research · 2017Article
- Corneal Expression of SLURP-1 by Age, Sex, Genetic Strain, and Ocular Surface Health.Investigative ophthalmology & visual science · 2015Article
- Therapeutic Use of Soluble Fas Ligand Ameliorates Acute and Recurrent Herpetic Stromal Keratitis in Mice.Investigative ophthalmology & visual science · 2015Article
- Decreased reactivation of a herpes simplex virus type 1 (HSV-1) latency-associated transcript (LAT) mutant using the in vivo mouse UV-B model of induced reactivation.Journal of neurovirology · 2015Article
- Anti-IL-17 therapy restricts and reverses late-term corneal allorejection.Journal of immunology (Baltimore, Md. : 1950) · 2015Article
- Impaired Fas-Fas Ligand Interactions Result in Greater Recurrent Herpetic Stromal Keratitis in Mice.Journal of immunology research · 2015Article
- SLURP-1 modulates corneal homeostasis by serving as a soluble scavenger of urokinase-type plasminogen activator.Investigative ophthalmology & visual science · 2014Article
- CXCL1 but not IL-6 is required for recurrent herpetic stromal keratitis.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Klf4 regulates the expression of Slurp1, which functions as an immunomodulatory peptide in the mouse cornea.Investigative ophthalmology & visual science · 2012Article
- Recurrent herpetic stromal keratitis in mice: a model for studying human HSK.Clinical & developmental immunology · 2012Review
Corrections and comments
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
Abstract
HSV-1 infection of the cornea leads to a potentially blinding immunoinflammatory lesion of the cornea, termed herpetic stromal keratitis. It has also been shown that one of the factors limiting inflammation of the cornea is the presence of Fas ligand (FasL) on corneal epithelium and endothelium. In this study, the role played by FasL expression in the cornea following acute infection with HSV-1 was determined. Both BALB/c and C57BL/6 (B6) mice with HSV-1 infection were compared with their lpr and gld counterparts. Results indicated that mice bearing mutations in the Fas Ag (lpr) displayed the most severe disease, whereas the FasL-defective gld mouse displayed an intermediate phenotype. It was further demonstrated that increased disease was due to lack of Fas expression on bone marrow-derived cells. Of interest, although virus persisted slightly longer in the corneas of mice bearing lpr and gld mutations, the persistence of infectious virus in the trigeminal ganglia was the same for all strains infected. Further, B6 mice bearing lpr and gld mutations were also more resistant to virus-induced mortality than were wild-type B6 mice. Thus, neither disease nor mortality correlated with viral replication in these mice. Collectively, the findings indicate that the presence of FasL on the cornea restricts the entry of Fas(+) bone marrow-derived inflammatory cells and thus reduces the severity of HSK.
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