ArticleInternational journal of inflammation2012
Resident Corneal Cells Communicate with Neutrophils Leading to the Production of IP-10 during the Primary Inflammatory Response to HSV-1 Infection.
Article in International journal of inflammation, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed, 15 citations in OpenAlex.
- The immunobiology of corneal HSV-1 infection and herpetic stromal keratitis.Clinical microbiology reviews · 2024Review
- Effect of resolvin D1 on experimental bacterial keratitis to prevent corneal scar.Graefe's archive for clinical and experimental ophthalmology = Albrecht von Graefes Archiv fur klinische und experimentelle Ophthalmologie · 2022Article
- IL-36γ induces a transient HSV-2 resistant environment that protects against genital disease and pathogenesis.Cytokine · 2018Article
- Inhibition of NUCKS Facilitates Corneal Recovery Following Alkali Burn.Scientific reports · 2017Article
- Prophylactic and therapeutic modulation of innate and adaptive immunity against mucosal infection of herpes simplex virus.Immune network · 2014Review
- CXCL1 but not IL-6 is required for recurrent herpetic stromal keratitis.Journal of immunology (Baltimore, Md. : 1950) · 2014Article
- Absence of CXCL10 aggravates herpes stromal keratitis with reduced primary neutrophil influx in mice.Journal of virology · 2013Article
- Immune response of T cells during herpes simplex virus type 1 (HSV-1) infection.Journal of Zhejiang University. Science. BReview
Corrections and comments
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Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
In this study we show that murine and human neutrophils are capable of secreting IP-10 in response to communication from the HSV-1 infected cornea and that they do so in a time frame associated with the recruitment of CD8(+) T cells and CXCR3-expressing cells. Cellular markers were used to establish that neutrophil influx corresponded in time to peak IP-10 production, and cellular depletion confirmed neutrophils to be a significant source of IP-10 during HSV-1 corneal infection in mice. A novel ex vivo model for human corneal tissue infection with HSV-1 was used to confirm that cells resident in the cornea are also capable of stimulating neutrophils to secrete IP-10. Our results support the hypothesis that neutrophils play a key role in T-cell recruitment and control of viral replication during HSV-1 corneal infection through the production of the T-cell recruiting chemokine IP-10.
Identifiers
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Registered trials
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.