ArticleThe Journal of investigative dermatology2012
The double-stranded RNA analogue polyinosinic-polycytidylic acid induces keratinocyte pyroptosis and release of IL-36γ.
Article in The Journal of investigative dermatology, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 54 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
54 citing papers in PubMed, 102 citations in OpenAlex.
- High Expression of IL-36γ in Influenza Patients Regulates Interferon Signaling Pathway and Causes Programmed Cell Death During Influenza Virus Infection.Frontiers in immunology · 2020Trial
- IL-36γ is a pivotal inflammatory player in periodontitis-associated bone loss.Scientific reports · 2019Trial
- Transcriptome Analysis of Porphyromonas gingivalis Lipopolysaccharide-Induced Early Gene Expression in Human Gingival Keratinocytes.Journal of periodontal research · 2025Article
- LL37 complexed to double-stranded RNA induces RIG-I-like receptor signalling and Gasdermin E activation facilitating IL-36γ release from keratinocytes.Cell death & disease · 2025Article
- The Central Roles of Keratinocytes in Coordinating Skin Immunity.The Journal of investigative dermatology · 2024Review
- Pap12-6: A host defense peptide with potent immunomodulatory activity in a chicken hepatic cell culture.PloS one · 2024Article
- Mpox virus infection and drug treatment modelled in human skin organoids.Nature microbiology · 2023Article
- Interleukin-36γ is causative for liver damage upon infection with Rift Valley fever virus in type I interferon receptor-deficient mice.Frontiers in immunology · 2023Article
- Treponema denticola Induces Interleukin-36γ Expression in Human Oral Gingival Keratinocytes via the Parallel Activation of NF-κB and Mitogen-Activated Protein Kinase Pathways.Infection and immunity · 2022Article
- Epithelial cells release IL-36α in extracellular vesicles following mechanical damage.Biochemical and biophysical research communications · 2022Article
- Enrichment of Tumor-Infiltrating B Cells in Group 4 Medulloblastoma in Children.International journal of molecular sciences · 2022Article
- Diverse Control Mechanisms of the Interleukin-1 Cytokine Family.Frontiers in cell and developmental biology · 2022Review
- L36G is associated with cutaneous antiviral competence in psoriasis.Frontiers in immunology · 2022Article
- IL-36 Cytokines: Their Roles in Asthma and Potential as a Therapeutic.Frontiers in immunology · 2022Review
- IL-36γ-armed oncolytic virus exerts superior efficacy through induction of potent adaptive antitumor immunity.Cancer immunology, immunotherapy : CII · 2021Article
- IL-36 cytokines and gut immunity.Immunology · 2021Review
- IL-36 in chronic inflammation and fibrosis - bridging the gap?The Journal of clinical investigation · 2021Review
- The Role of IL-36 in Infectious Diseases: Potential Target for COVID-19?Frontiers in immunology · 2021Review
- Interleukin-36: Structure, Signaling and Function.Advances in experimental medicine and biology · 2021Review
- Adjuvanting Allergen Extracts for Sublingual Immunotherapy: Calcitriol Downregulates CXCL8 Production in Primary Sublingual Epithelial Cells.Frontiers in immunology · 2020Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
IL-36 is the common name for the three IL-1 family members IL-36α, IL-36β, and IL-36γ, formerly known as IL-1F6, IL-1F8, and IL-1F9, respectively. IL-36 appears to have pro-inflammatory activities; however, the physiological function of these cytokines remains unknown. Expression of IL-36 by keratinocytes implies its possible involvement in innate immune responses in the skin. We observed that, of the three IL-36 isoforms, human keratinocytes express high levels of IL-36γ. IL-36γ mRNA expression was dramatically induced by the Toll-like receptor ligands polyinosinic-polycytidylic acid (poly(I:C)) and flagellin. Surprisingly, the IL-36γ protein was released by cells treated with poly(I:C), but remained intracellular in cells treated with flagellin only. poly(I:C), but not flagellin, induced cell death and caspase-3/7 activation. Inhibition of caspase-3/7 and caspase-1 blocked extracellular release of IL-36γ from poly(I:C)-treated cells. Furthermore, caspase-1 inhibition prevented poly(I:C)-induced caspase-3/7 activation. Interestingly, transcription of the gene IL36G was dependent on caspase-1, but not caspase-3/7, activation. This demonstrates that the pathways leading to IL36G transcription and caspase-3/7 activation branch after caspase-1. This divergence of the pathways allows the cells to enter a state of de novo protein synthesis before committing to pyroptosis. Overall, our observations suggest that IL-36γ may be an alarmin that signals the cause, e.g., viral infection, of cell death.
Indexed as
Identifiers
What OpenQuestion holds
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.