ArticleScientific reports2018
Interleukin-33 is activated by allergen- and necrosis-associated proteolytic activities to regulate its alarmin activity during epithelial damage.
Article in Scientific reports, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 papers.
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Who cites it
73 citing papers in PubMed, 109 citations in OpenAlex.
- Population pharmacokinetic/target engagement modelling of tozorakimab in healthy volunteers and patients with chronic obstructive pulmonary disease.British journal of clinical pharmacology · 2024Trial
- Interleukin-33 and its receptor: multifaceted roles and emerging therapeutic potential.Nature reviews. Immunology · 2026Review
- Rewiring Atopic Dermatitis: Alarmin Cytokines at the Core of Barrier-Immune-Neuro-Microbiome Networks.Clinical reviews in allergy & immunology · 2026Review
- Mast cells and endothelial cells mediate interleukin-33 and ST2 responses in distal chronic obstructive pulmonary disease lungs.American journal of respiratory and critical care medicine · 2026Article
- Screening and Engineering of Hetero-Bivalent Nanobody Targeting Interleukin-33 with Enhanced Binding Stability.Biomolecules · 2026Article
- Cathepsin C orchestrates RSV-induced asthma exacerbation through the dual effect of monocyte-derived macrophages.Cellular & molecular immunology · 2026Article
- Platelet-macrophage cooperation drives IL-33-dependent type 2 lung immunopathology in a sex-biased manner.The Journal of allergy and clinical immunology · 2026Article
- Ginsenoside Rg1 attenuates asthma features in mice co-exposed to house dust mite allergen and diesel exhaust particle by modulating epithelial ILC2 interactions.Journal of ginseng research · 2026Article
- Pro-inflammatory and counter-regulatory modulators of interleukin-5-driven eosinophil programs: a framework for precision medicine in eosinophilic diseases.Frontiers in immunology · 2026Review
- Immunotherapy for asthma.Cellular & molecular immunology · 2025Review
- Hepatitis B virus promotes liver cancer by modulating the immune response to environmental carcinogens.Nature communications · 2025Article
- IL-33 is associated with alveolar dysfunction in patients with viral lower respiratory tract disease.Mucosal immunology · 2025Article
- Type 2 immunity in allergic diseases.Cellular & molecular immunology · 2025Review
- Article
- Full-length and N-terminally truncated recombinant interleukin-38 variants are similarly inefficient in antagonizing interleukin-36 and interleukin-1 receptors.Cell communication and signaling : CCS · 2025Article
- Epithelial-derived cytokines in the pathogenesis of severe asthma.Frontiers in allergy · 2025Review
- Epithelial Interleukin-1 Receptor-Like-1 Activation Is Contingent on Interleukin-33 Isoforms and Asthma-Related Receptor Variation.Clinical and experimental allergy : journal of the British Society for Allergy and Clinical Immunology · 2024Article
- Epithelial sensing in allergic disease.Current opinion in immunology · 2024Review
- Therapeutic monoclonal antibodies in allergy: Targeting IgE, cytokine, and alarmin pathways.Immunological reviews · 2024Review
- Targeted proteomics of cerebrospinal fluid in treatment naïve multiple sclerosis patients identifies immune biomarkers of clinical phenotypes.Scientific reports · 2024Article
13 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Interleukin (IL)-33 is an IL-1 family alarmin released from damaged epithelial and endothelial barriers to elicit immune responses and allergic inflammation via its receptor ST2. Serine proteases released from neutrophils, mast cells and cytotoxic lymphocytes have been proposed to process the N-terminus of IL-33 to enhance its activity. Here we report that processing of full length IL-33 can occur in mice deficient in these immune cell protease activities. We sought alternative mechanisms for the proteolytic activation of IL-33 and discovered that exogenous allergen proteases and endogenous calpains, from damaged airway epithelial cells, can process full length IL-33 and increase its alarmin activity up to ~60-fold. Processed forms of IL-33 of apparent molecular weights ~18, 20, 22 and 23 kDa, were detected in human lungs consistent with some, but not all, proposed processing sites. Furthermore, allergen proteases degraded processed forms of IL-33 after cysteine residue oxidation. We suggest that IL-33 can sense the proteolytic and oxidative microenvironment during tissue injury that facilitate its rapid activation and inactivation to regulate the duration of its alarmin function.
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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.