ArticleThe American journal of pathology2016
IL-19 Halts Progression of Atherosclerotic Plaque, Polarizes, and Increases Cholesterol Uptake and Efflux in Macrophages.
Article in The American journal of pathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 35 papers.
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Who cites it
35 citing papers in PubMed, 48 citations in OpenAlex.
- Suppression of macrophage membrane cholesterol efflux by SLAMF7-induced IL-7 signaling improves immunotherapy efficacy in hepatocellular carcinoma.Hepatology international · 2026Article
- Integrative transcriptomic analysis identifies ACP5 and FBLN5 as candidate shared transcriptomic signatures between pulpitis and carotid plaque rupture.Scientific reports · 2026Article
- Harnessing macrophage signaling pathways and scalable engineering for next-generation immunotherapies.Signal transduction and targeted therapy · 2026Review
- Reprogramming macrophage metabolism for cardiovascular therapy: From molecular pathways to precision nanomedicine.Materials today. Bio · 2026Review
- Macrophages tune responses to pathogen dynamics through TLR4 stimulation memory and by licensing susceptibility to IL-10.bioRxiv : the preprint server for biology · 2026Article
- Anti-Inflammatory Interleukins in the Pathogenesis of Atherosclerosis.International journal of molecular sciences · 2026Review
- Single-cell and spatial transcriptomics map senescent vascular cells in arterial remodeling during atherosclerosis in mice.Nature aging · 2025Article
- IL-19 Is a Novel Lymphangiocrine Factor Inducing Lymphangiogenesis and Lymphatic Junctional Regulation.Arteriosclerosis, thrombosis, and vascular biology · 2025Article
- The signature based on interleukin family and receptors identified IL19 and IL20RA in promoting nephroblastoma progression through STAT3 pathway.Scientific reports · 2025Article
- IL-19 suppresses Hippo signaling via modulating YAP1 phosphorylation in osteoarthritis.Frontiers in immunology · 2025Article
- Macrophages in cardiovascular diseases: molecular mechanisms and therapeutic targets.Signal transduction and targeted therapy · 2024Review
- DPP4 inhibition impairs senohemostasis to improve plaque stability in atherosclerotic mice.The Journal of clinical investigation · 2023Article
- FXR1 regulates vascular smooth muscle cell cytoskeleton, VSMC contractility, and blood pressure by multiple mechanisms.Cell reports · 2023Article
- Macrophage polarization states in atherosclerosis.Frontiers in immunology · 2023Review
- Interleukin-19 Promotes Retinal Neovascularization in a Mouse Model of Oxygen-Induced Retinopathy.Investigative ophthalmology & visual science · 2022Article
- Deletion of LDLRAP1 Induces Atherosclerotic Plaque Formation, Insulin Resistance, and Dysregulated Insulin Response in Adipose Tissue.The American journal of pathology · 2022Article
- Review
- Recombinant Interleukin-19 Suppresses the Formation and Progression of Experimental Abdominal Aortic Aneurysms.Journal of the American Heart Association · 2021Article
- The Crucial Role of PPARγ-Egr-1-Pro-Inflammatory Mediators Axis in IgG Immune Complex-Induced Acute Lung Injury.Frontiers in immunology · 2021Article
- Macrophage Plasticity and Atherosclerosis Therapy.Frontiers in molecular biosciences · 2021Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Atherosclerosis regression is an important clinical goal, and treatments that can reverse atherosclerotic plaque formation are actively being sought. Our aim was to determine whether administration of exogenous IL-19, a Th2 cytokine, could attenuate progression of preformed atherosclerotic plaque and to identify molecular mechanisms. LDLR(-/-) mice were fed a Western diet for 12 weeks, then administered rIL-19 or phosphate-buffered saline concomitant with Western diet for an additional 8 weeks. Analysis of atherosclerosis burden showed that IL-19-treated mice were similar to baseline, in contrast to control mice which showed a 54% increase in plaque, suggesting that IL-19 halted the progression of atherosclerosis. Plaque characterization showed that IL-19-treated mice had key features of atherosclerosis regression, including a reduction in macrophage content and an enrichment in markers of M2 macrophages. Mechanistic studies revealed that IL-19 promotes the activation of key pathways leading to M2 macrophage polarization, including STAT3, STAT6, Kruppel-like factor 4, and peroxisome proliferator-activated receptor γ, and can reduce cytokine-induced inflammation in vivo. We identified a novel role for IL-19 in regulating macrophage lipid metabolism through peroxisome proliferator-activated receptor γ-dependent regulation of scavenger receptor-mediated cholesterol uptake and ABCA1-mediated cholesterol efflux. These data show that IL-19 can halt progression of preformed atherosclerotic plaques by regulating both macrophage inflammation and cholesterol homeostasis and implicate IL-19 as a link between inflammation and macrophage cholesterol metabolism.
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Registered trials
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