ArticleCommunications biology2021
IL36 is a critical upstream amplifier of neutrophilic lung inflammation in mice.
Article in Communications biology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
What it found
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Who cites it
27 citing papers in PubMed, 50 citations in OpenAlex.
- IL-36 activates neutrophil extracellular traps and exacerbates LPS-induced ARDS in mice.Scientific reports · 2026Article
- Mucosal IL-36 is a defining feature of severe paediatric bronchiolitis.Mucosal immunology · 2026Article
- Neutrophil-derived exosomes inhibit gastric cancer progression via miR-101-3p-mediated suppression of MCL1.Cancer cell international · 2026Article
- Preceding influenza infection impacts neutrophil response to Aspergillus fumigatus and Staphylococcus aureus.ImmunoHorizons · 2025Article
- The role of fibroblast-neutrophil crosstalk in the pathogenesis of inflammatory diseases: a multi-tissue perspective.Frontiers in immunology · 2025Review
- UBE2N Is Essential for Maintenance of Skin Homeostasis and Suppression of Inflammation.The Journal of investigative dermatology · 2024Article
- Perinatal Caffeine Administration Improves Outcomes in an Ovine Model of Neonatal Hypoxia-Ischemia.Stroke · 2024Article
- The impact of the tumor microenvironment on the survival of penile cancer patients.Scientific reports · 2024Article
- Interleukin-1 receptor accessory protein blockade limits the development of atherosclerosis and reduces plaque inflammation.Cardiovascular research · 2024Article
- FloxedCells · 2024Article
- Inflammation as the nexus: exploring the link between acute myocardial infarction and chronic obstructive pulmonary disease.Frontiers in cardiovascular medicine · 2024Review
- Monocyte-derived alveolar macrophages are key drivers of smoke-induced lung inflammation and tissue remodeling.Frontiers in immunology · 2024Article
- UBE2N is essential for maintenance of skin homeostasis and suppression of inflammation.bioRxiv : the preprint server for biology · 2023Article
- Luteolin alleviated neutrophilic asthma by inhibiting IL-36γ secretion-mediated MAPK pathways.Pharmaceutical biology · 2023Article
- Article
- IL-36α inhibits melanoma by inducing pro-inflammatory polarization of macrophages.Cancer immunology, immunotherapy : CII · 2023Article
- Autonomous IL-36R signaling in neutrophils activates potent antitumor effector functions.The Journal of clinical investigation · 2023Article
- Macrophages in Skin Wounds: Functions and Therapeutic Potential.Biomolecules · 2022Review
- IL-36 receptor agonist and antagonist imbalance drives neutrophilic inflammation in COPD.JCI insight · 2022Article
- Regulation of Interleukin-36γ/IL-36R Signaling Axis by PIN1 in Epithelial Cell Transformation and Breast Tumorigenesis.Cancers · 2022Article
Corrections and comments
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Authors and funding
17 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
IL-36, which belongs to the IL-1 superfamily, is increasingly linked to neutrophilic inflammation. Here, we combined in vivo and in vitro approaches using primary mouse and human cells, as well as, acute and chronic mouse models of lung inflammation to provide mechanistic insight into the intercellular signaling pathways and mechanisms through which IL-36 promotes lung inflammation. IL-36 receptor deficient mice exposed to cigarette smoke or cigarette smoke and H1N1 influenza virus had attenuated lung inflammation compared with wild-type controls. We identified neutrophils as a source of IL-36 and show that IL-36 is a key upstream amplifier of lung inflammation by promoting activation of neutrophils, macrophages and fibroblasts through cooperation with GM-CSF and the viral mimic poly(I:C). Our data implicate IL-36, independent of other IL-1 family members, as a key upstream amplifier of neutrophilic lung inflammation, providing a rationale for targeting IL-36 to improve treatment of a variety of neutrophilic lung diseases.
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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.