ArticleNature communications2014
Interleukin-1α released from HSV-1-infected keratinocytes acts as a functional alarmin in the skin.
Article in Nature communications, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 33 papers.
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
33 citing papers in PubMed, 51 citations in OpenAlex.
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- HSV-1 inhibits melanogenesis of PIG1 cells through downregulation of VN1R5/ERK pathway.Archives of dermatological research · 2025Article
- Co-infection of HSV-1 amplicons containing theBiochemistry and biophysics reports · 2024Article
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- System analysis based on the pyroptosis-related genes identifes GSDMD as a novel therapy target for skin cutaneous melanoma.Journal of translational medicine · 2023Article
- Pellino Proteins in Viral Immunity and Pathogenesis.Viruses · 2023Review
- The Intersection of Innate Immune Pathways with the Latent Herpes Simplex Virus Genome.Journal of virology · 2023Review
- Pellino1 Restricts Herpes Simplex Virus Infections in the Epidermis and Dissemination to Sebaceous Glands.The Journal of investigative dermatology · 2023Article
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- Cytokines and chemokines: The vital role they play in herpes simplex virus mucosal immunology.Frontiers in immunology · 2022Review
- HMGB1-mediated chromatin remodeling attenuatesProceedings of the National Academy of Sciences of the United States of America · 2021Article
- Crosstalk Between Epithelial Cells, Neurons and Immune Mediators in HSV-1 Skin Infection.Frontiers in immunology · 2021Review
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- Comparative analysis of the tear protein profile in herpes simplex virus type 1 epithelial keratitis.BMC ophthalmology · 2020Article
- Programmed Cell Death in the Evolutionary Race against Bacterial Virulence Factors.Cold Spring Harbor perspectives in biology · 2020Review
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 1 country.
Funding
Abstract
Herpes simplex virus-1 (HSV-1) is a human pathogen that utilizes several strategies to circumvent the host immune response. An immune evasion mechanism employed by HSV-1 is retention of interleukin-1β (IL-1β) in the intracellular space, which blocks the pro-inflammatory activity of IL-1β. Here we report that HSV-1-infected keratinocytes actively release the also pro-inflammatory IL-1α, preserving the ability of infected cells to signal danger to the surrounding tissue. The extracellular release of IL-1α is independent of inflammatory caspases. In vivo recruitment of leukocytes to early HSV-1 microinfection sites within the epidermis is dependent upon IL-1 signalling. Following cutaneous HSV-1 infection, mice unable to signal via extracellular IL-1α exhibit an increased mortality rate associated with viral dissemination. We conclude that IL-1α acts as an alarmin essential for leukocyte recruitment and protective immunity against HSV-1. This function may have evolved to counteract an immune evasion mechanism deployed by HSV-1.
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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.