ArticleFrontiers in immunology2022
The atypical chemokine receptor-2 fine-tunes the immune response in herpes stromal keratitis.
Article in Frontiers in immunology, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 4 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
4 citing papers in PubMed, 5 citations in OpenAlex.
- Research progress on the correlation between corneal neovascularization and lymphangiogenesis (Review).Molecular medicine reports · 2025Review
- Methylation in cornea and corneal diseases: a systematic review.Cell death discovery · 2024Review
- Herpes simplex keratitis: A brief clinical overview.World journal of virology · 2024Review
- New targets of nascent lymphatic vessels in ocular diseases.Frontiers in physiology · 2024Review
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Authors and funding
6 authors at 3 institutions in 3 countries.
Funding
Abstract
Herpes stromal keratitis (HSK) is a blinding corneal disease caused by herpes simplex virus-1 (HSV-1), a common pathogen infecting most of the world's population. Inflammation in HSK is chemokine-dependent, particularly CXCL10 and less so the CC chemokines. The atypical chemokine receptor-2 (ACKR2) is a decoy receptor predominantly for pro-inflammatory CC chemokines, which regulates the inflammatory response by scavenging inflammatory chemokines thereby modulating leukocyte infiltration. Deletion of ACKR2 exacerbates and delays the resolution of the inflammatory response in most models. ACKR2 also regulates lymphangiogenesis and mammary duct development through the recruitment of tissue-remodeling macrophages. Here, we demonstrate a dose-dependent upregulation of ACKR2 during corneal HSV-1 infection. At an HSV inoculum dose of 5.4 x 10
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