ArticleCellular immunology2023
Full-length IL-33 augments pulmonary fibrosis in an ST2- and Th2-independent, non-transcriptomic fashion.
Article in Cellular immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 10 papers.
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Who cites it
10 citing papers in PubMed, 8 citations in OpenAlex.
- Blocking interleukin 33 reduces joint, systemic, and lung inflammatory responses in the combined collagen-induced arthritis-inhalant endotoxin exposure model.The Journal of pharmacology and experimental therapeutics · 2026Article
- Fibrotic chronic eosinophilic pneumonia: from inflammation to fibrosis and therapeutic implications.European respiratory review : an official journal of the European Respiratory Society · 2026Review
- Beyond inflammation: alarmins as critical drivers of pulmonary fibrosis.ERJ open research · 2026Review
- Multi-omics integration and machine learning reveal gut-immune signatures in idiopathic pulmonary fibrosis: insights from bulk RNA-seq, single-cell profiles, spatial transcriptomics, and experimental validation.Frontiers in immunology · 2026Article
- Activation of TSLP-IL-9 Axis Hinders the Antifibrotic Effect of ST2 Deficiency in Pulmonary Fibrosis.International journal of molecular sciences · 2025Article
- Therapeutic targeting of full-length interleukin-33 protein levels with cell-permeable decoy peptides attenuates fibrosis in the bleomycin model in vivo.The Journal of pharmacology and experimental therapeutics · 2025Article
- The IL-33/ST2 Axis Is Not Required for the Profibrotic Effect of IL-33 in the Lungs.American journal of respiratory cell and molecular biology · 2024Article
- Unveiling the multifaceted antitumor effects of interleukin 33.Frontiers in immunology · 2024Review
- The production, function, and clinical applications of IL-33 in type 2 inflammation-related respiratory diseases.Frontiers in immunology · 2024Review
- Unpacking the complexity of nuclear IL-33 (nIL-33): a crucial regulator of transcription and signal transduction.Journal of cell communication and signaling · 2023Review
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Authors and funding
12 authors at 2 institutions in 1 country.
Funding
Abstract
Mature IL-33 (MIL33) acting through its receptor, ST2, is known to regulate fibrosis. The precursor, full-length IL-33 (FLIL33), may function differently from MIL33 and independently of ST2. Here we report that genetic deletion of either IL-33 or ST2 attenuates pulmonary fibrosis in the bleomycin model, as does Cre-induced IL-33 deficiency in response to either acute or chronic bleomycin challenge. However, adenovirus-mediated gene delivery of FLIL33, but not MIL33, to the lungs of either wild-type or ST2-deficient mice potentiates the profibrotic effect of bleomycin without inducing a Th2 phenotype. In cultured mouse lung cells, FLIL33 overexpression induces moderate and distinct transcriptomic changes compared with a robust response induced by MIL33, whereas ST2 deletion abrogates the effects of both IL-33 forms. Thus, FLIL33 may contribute to fibrosis in an ST2-independent, Th2-independent, non-transcriptomic fashion, suggesting that pharmacological targeting of both FLIL33 and MIL33 may prove efficacious in patients with pulmonary fibrosis.
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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.