ArticleThe Journal of biological chemistry2014
IFN-γ directly controls IL-33 protein level through a STAT1- and LMP2-dependent mechanism.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 32 papers.
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Who cites it
32 citing papers in PubMed, 41 citations in OpenAlex.
- Non-Invasive Biomarkers for Assessing Liver Fibrosis in Biliary Atresia: A Literature Review.International journal of molecular sciences · 2026Review
- Influenza A/PR8 virus infection in mice suppresses basal and Oncostatin M-induced IL-33 expression in vivo and in vitro.Scientific reports · 2026Article
- ERα activates NAMPT/IL-33 signaling to enhance beige thermogenesis and metabolic fitness.Science advances · 2026Article
- Potential Inflammatory Mediators in Pericardial Fluids of Patients With Coronary Artery Diseases and Their Association With Plasma Biomarkers.Journal of cellular and molecular medicine · 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
- Keloids and inflammation: the crucial role of IL-33 in epidermal changes.Frontiers in immunology · 2025Article
- Age-dependent Pdgfrβ signaling drives adipocyte progenitor dysfunction to alter the beige adipogenic niche in male mice.Nature communications · 2023Article
- Full-length IL-33 augments pulmonary fibrosis in an ST2- and Th2-independent, non-transcriptomic fashion.Cellular immunology · 2023Article
- Wild-type S100A3 and S100A13 restore calcium homeostasis and mitigate mitochondrial dysregulation in pulmonary fibrosis patient-derived cells.Frontiers in cell and developmental biology · 2023Article
- Interleukin (IL)-33 immunobiology in asthma and airway inflammatory diseases.The Journal of asthma : official journal of the Association for the Care of Asthma · 2022Article
- Review
- Ischemia reperfusion injury facilitates lung allograft acceptance through IL-33-mediated activation of donor-derived IL-5 producing group 2 innate lymphoid cells.American journal of transplantation : official journal of the American Society of Transplantation and the American Society of Transplant Surgeons · 2022Article
- Immunopathological signatures in multisystem inflammatory syndrome in children and pediatric COVID-19.Nature medicine · 2022Article
- Natural Compounds Tapinarof andFrontiers in immunology · 2022Article
- A Pilot Clinical Study of Hyperacute Serum Treatment in Osteoarthritic Knee Joint: Cytokine Changes and Clinical Effects.Current issues in molecular biology · 2021Article
- The blockade of interleukin-33 released by hepatectomy would be a promising treatment option for cholangiocarcinoma.Cancer science · 2021Article
- Full-length IL-33 regulates Smad3 phosphorylation and gene transcription in a distinctive AP2-dependent manner.Cellular immunology · 2020Article
- IL-33 Mediates Lung Inflammation by the IL-6-Type Cytokine Oncostatin M.Mediators of inflammation · 2020Article
- Contributions of IL-33 in Non-hematopoietic Lung Cells to Obstructive Lung Disease.Frontiers in immunology · 2020Review
- DAMPs in Unilateral Ureteral Obstruction.Frontiers in immunology · 2020Review
Corrections and comments
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
Abstract
IL-33 contributes to disease processes in association with Th1 and Th2 phenotypes. IL-33 mRNA is rapidly regulated, but the fate of synthesized IL-33 protein is unknown. To understand the interplay among IL-33, IFN-γ, and IL-4 proteins, recombinant replication-deficient adenoviruses were produced and used for dual expression of IL-33 and IFN-γ or IL-33 and IL-4. The effects of such dual gene delivery were compared with the effects of similar expression of each of these cytokines alone. In lung fibroblast culture, co-expression of IL-33 and IFN-γ resulted in suppression of the levels of both proteins, whereas co-expression of IL-33 and IL-4 led to mutual elevation. In vivo, co-expression of IL-33 and IFN-γ in the lungs led to attenuation of IL-33 protein levels. Purified IFN-γ also attenuated IL-33 protein in fibroblast culture, suggesting that IFN-γ controls IL-33 protein degradation. Specific inhibition of caspase-1, -3, and -8 had minimal effect on IFN-γ-driven IL-33 protein down-regulation. Pharmacological inhibition, siRNA-mediated silencing, or gene deficiency of STAT1 potently up-regulated IL-33 protein expression levels and attenuated the down-regulating effect of IFN-γ on IL-33. Stimulation with IFN-γ strongly elevated the levels of the LMP2 proteasome subunit, known for its role in IFN-γ-regulated antigen processing. siRNA-mediated silencing of LMP2 expression abrogated the effect of IFN-γ on IL-33. Thus, IFN-γ, IL-4, and IL-33 are engaged in a complex interplay. The down-regulation of IL-33 protein levels by IFN-γ in pulmonary fibroblasts and in the lungs in vivo occurs through STAT1 and non-canonical use of the LMP2 proteasome subunit in a caspase-independent fashion.
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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.