ArticleMucosal immunology2017
IL-36 receptor deletion attenuates lung injury and decreases mortality in murine influenza pneumonia.
Article in Mucosal immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 38 papers.
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Who cites it
38 citing papers in PubMed, 71 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
- Innate immune circuits in acute lung injury: macrophage plasticity, ILC crosstalk, and tissue repair failure.Frontiers in immunology · 2026Review
- Influence of serum IL-36 subfamily cytokines on clinical manifestations of asthma.The journal of allergy and clinical immunology. Global · 2025Article
- Review
- Transcriptome Analysis of Porphyromonas gingivalis Lipopolysaccharide-Induced Early Gene Expression in Human Gingival Keratinocytes.Journal of periodontal research · 2025Article
- Advances in understanding the role of interleukins in pulmonary fibrosis (Review).Experimental and therapeutic medicine · 2025Review
- FloxedCells · 2024Article
- Emerging functions and therapeutic targets of IL-38 in central nervous system diseases.CNS neuroscience & therapeutics · 2024Review
- The pathogenesis of influenza in intact alveoli: virion endocytosis and its effects on the lung's air-blood barrier.Frontiers in immunology · 2024Review
- Interleukin-36 Receptor Signaling Attenuates Epithelial Wound Healing in C57BL/6 Mouse Corneas.Cells · 2023Article
- Article
- IL-36 receptor agonist and antagonist imbalance drives neutrophilic inflammation in COPD.JCI insight · 2022Article
- Epithelial cells release IL-36α in extracellular vesicles following mechanical damage.Biochemical and biophysical research communications · 2022Article
- The Protective Role of IL-36/IL-36R Signal in Con A-Induced Acute Hepatitis.Journal of immunology (Baltimore, Md. : 1950) · 2022Article
- IL-36 Cytokines: Their Roles in Asthma and Potential as a Therapeutic.Frontiers in immunology · 2022Review
- IL-36α Enhances Host Defense againstJournal of immunology (Baltimore, Md. : 1950) · 2021Article
- Analysis of Il36a induction by C/EBPβ via a half-CRE•C/EBP element in murine macrophages in dependence of its CpG methylation level.Genes and immunity · 2021Article
- IL-36 cytokines in inflammatory and malignant diseases: not the new kid on the block anymore.Cellular and molecular life sciences : CMLS · 2021Review
- IL-36 cytokines and gut immunity.Immunology · 2021Review
- Role of IL-36γ/IL-36R Signaling in Corneal Innate Defense Against Candida albicans Keratitis.Investigative ophthalmology & visual science · 2021Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Influenza virus causes a respiratory disease in humans that can progress to lung injury with fatal outcome. The interleukin (IL)-36 cytokines are newly described IL-1 family cytokines that promote inflammatory responses via binding to the IL-36 receptor (IL-36R). The mechanism of expression and the role of IL-36 cytokines are poorly understood. Here, we investigated the role of IL-36 cytokines in modulating the innate inflammatory response during influenza virus-induced pneumonia in mice. The intranasal administration of influenza virus upregulated IL-36α mRNA and protein production in the lungs. In vitro, influenza virus-mediated IL-36α but not IL-36γ is induced and secreted from alveolar epithelial cells (AECs) through both a caspase-1 and caspase-3/7 dependent pathway. IL-36α was detected in microparticles shed from AECs and promoted the production of pro-inflammatory cytokines and chemokines in respiratory cells. IL-36R-deficient mice were protected from influenza virus-induced lung injury and mortality. Decreased mortality was associated with significantly reduced early accumulation of neutrophils and monocytes/macrophages, activation of lymphocytes, production of pro-inflammatory cytokines and chemokines, and permeability of the alveolar-epithelial barrier in despite impaired viral clearance. Taken together, these data indicate that IL-36 ligands exacerbate lung injury during influenza virus infection.
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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.