ArticleJournal of immunology (Baltimore, Md. : 1950)2011
Role of IL-17 and Th17 cells in herpes simplex virus-induced corneal immunopathology.
Article in Journal of immunology (Baltimore, Md. : 1950), 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 103 papers, 1 of them a synthesis that pooled it.
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Who cites it
103 citing papers in PubMed, 1 synthesis or guideline pooled it, 151 citations in OpenAlex.
- Role of Neutrophils on the Ocular Surface.International journal of molecular sciences · 2021Pooled it
- An analysis of regulatory T-cell and Th-17 cell dynamics during cytomegalovirus replication in solid organ transplant recipients.PloS one · 2012Trial
- Optineurin restrains IL-17-associated neuroinflammation in trigeminal ganglia to preserve sensory function after ocular HSV-1 infection.Journal of immunology (Baltimore, Md. : 1950) · 2026Article
- Molecular Pathways Driving Corneal Neovascularization in Herpes Simplex Keratitis.Pathogens (Basel, Switzerland) · 2026Review
- Antagonizing Viral MicroRNAs Reduces Ocular HSV-1 Pathogenesis and Enhances Mucosal Immune Homeostasis.Investigative ophthalmology & visual science · 2025Article
- Herpes stromal keratitis erodes the establishment of tissue-resident memory T cell pool in HSV-1 infected corneas.Mucosal immunology · 2025Article
- γδ T17 Cells Regulate the Acute Antiviral Response of NK Cells in HSV-1-Infected Corneas.Investigative ophthalmology & visual science · 2024Article
- The immunobiology of corneal HSV-1 infection and herpetic stromal keratitis.Clinical microbiology reviews · 2024Review
- Article
- Methylation in cornea and corneal diseases: a systematic review.Cell death discovery · 2024Review
- Meeting the Challenge of Controlling Viral Immunopathology.International journal of molecular sciences · 2024Review
- Role of IL-27 in HSV-1-Induced Herpetic Stromal Keratitis.Journal of immunology (Baltimore, Md. : 1950) · 2023Article
- An ocular Th1 immune response promotes corneal nerve damage independently of the development of corneal epitheliopathy.Journal of neuroinflammation · 2023Article
- Role of Innate Interferon Responses at the Ocular Surface in Herpes Simplex Virus-1-Induced Herpetic Stromal Keratitis.Pathogens (Basel, Switzerland) · 2023Review
- Controlling viral inflammatory lesions by rebalancing immune response patterns.Frontiers in immunology · 2023Review
- Association of Single-Nucleotide Polymorphisms in Interleukin Genes with Microbial Keratitis in a South Indian Population.Pathogens (Basel, Switzerland) · 2022Article
- The potential roles of interleukin-25 in infectious diseases.Frontiers in immunology · 2022Review
- Cytokines and chemokines: The vital role they play in herpes simplex virus mucosal immunology.Frontiers in immunology · 2022Review
- Modulating glutamine metabolism to control viral immuno-inflammatory lesions.Cellular immunology · 2021Article
- Interleukin-17-A multifaceted cytokine in viral infections.Journal of cellular physiology · 2021Review
43 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
7 authors at 3 institutions in 1 country.
Funding
Abstract
HSV-1 infection of the cornea leads to a blinding immunoinflammatory lesion of the eye termed stromal keratitis (SK). Recently, IL-17-producing CD4(+) T cells (Th17 cells) were shown to play a prominent role in many autoimmune conditions, but the role of IL-17 and/or of Th17 cells in virus immunopathology is unclear. In this study, we show that, after HSV infection of the cornea, IL-17 is upregulated in a biphasic manner with an initial peak production around day 2 postinfection and a second wave starting from day 7 postinfection with a steady increase until day 21 postinfection, a time point when clinical lesions are fully evident. Further studies demonstrated that innate cells, particularly γδ T cells, were major producers of IL-17 early after HSV infection. However, during the clinical phase of SK, the predominant source of IL-17 was Th17 cells that infiltrated the cornea only after the entry of Th1 cells. By ex vivo stimulation, the half fraction of IFN-γ-producing CD4(+) T cells (Th1 cells) were HSV specific, whereas very few Th17 cells responded to HSV stimulation. The delayed influx of Th17 cells in the cornea was attributed to the local chemokine and cytokine milieu. Finally, HSV infection of IL-17R knockout mice as well as IL-17 neutralization in wild-type mice showed diminished SK severity. In conclusion, our results show that IL-17 and Th17 cells contribute to the pathogenesis of SK, the most common cause of infectious blindness in the Western world.
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Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.