ArticleFree radical biology & medicine2013
IL-4 and IL-13 employ discrete signaling pathways for target gene expression in alternatively activated monocytes/macrophages.
Article in Free radical biology & medicine, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 139 papers.
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Who cites it
139 citing papers in PubMed, 233 citations in OpenAlex.
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- The mechanism of action and therapeutic potential of macrophages in osteoporosis: from polarization balance to targeted regulation.Frontiers in immunology · 2026Review
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- Obesity and type 2 diabetes as chronic inflammation: how does the cytokine evidence align?Frontiers in endocrinology · 2026Review
- High-Dimensional Profiling of Circulating Dendritic Cells and Monocytes in Atopic Dermatitis Patients by Mass Cytometry.Allergy, asthma & immunology research · 2026Article
- Reversal of filarial serpin Wb123-urokinase plasminogen activator receptor mediated alternative macrophage activation by monoclonal antibody.PLoS neglected tropical diseases · 2025Article
- Article
- Differential regulation of 5-lipoxygenase and leukotriene-C4-synthase expression by IFNγ, IL-4 and IL-13 in human monocytes and macrophages from patients with atopic dermatitis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025Article
- Growth differentiation factor 11 modulates metabolism, mitigating the pro-tumoral behavior provided by M2-like macrophages in hepatocellular carcinoma-derived cells.World journal of gastroenterology · 2025Article
- Cold Plasma Generates a Localized Inflammatory Response and Promotes Muscle Repair.Advanced therapeutics · 2025Article
- Adrenomedullin-RAMP2 System Modulates Inflammation and Tissue Repair in Experimental Autoimmune Uveitis Via T-Cell and M2 Macrophage Regulation.Investigative ophthalmology & visual science · 2025Article
- 4-fluorophenylacetamide acetyl coumarin induces pro-inflammatory M1 macrophage polarization and suppresses the immunosuppressive M2 phenotype through PI3k/AKT/NF-κB modulation.Molecular biology reports · 2025Article
- Inflammation and Prediction of Death in Type 2 Diabetes. Evidence of an Intertwined Link With Tryptophan Metabolism.The Journal of clinical endocrinology and metabolism · 2025Article
- Neuroinflammation and Amyotrophic Lateral Sclerosis: Recent Advances in Anti-Inflammatory Cytokines as Therapeutic Strategies.International journal of molecular sciences · 2025Review
79 more citing papers are in PubMed but not listed here.
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Monocytes/macrophages are innate immune cells that play a crucial role in the resolution of inflammation. In the presence of the Th2 cytokines interleukin-4 (IL-4) and interleukin-13 (IL-13), they display an anti-inflammatory profile and this activation pathway is known as alternative activation. In this study we compare and differentiate pathways mediated by IL-4 and IL-13 activation of human monocytes/macrophages. Here we report differential regulation of IL-4 and IL-13 signaling in monocytes/macrophages starting from IL-4/IL-13 cytokine receptors to Jak/Stat-mediated signaling pathways that ultimately control expression of several inflammatory genes. Our data demonstrate that although the receptor-associated tyrosine kinases Jak2 and Tyk2 are activated after the recruitment of IL-13 to its receptor (containing IL-4Rα and IL-13Rα1), IL-4 stimulates Jak1 activation. We further show that Jak2 is upstream of Stat3 activation and Tyk2 controls Stat1 and Stat6 activation in response to IL-13 stimulation. In contrast, Jak1 regulates Stat3 and Stat6 activation in IL-4-induced monocytes. Our results further reveal that although IL-13 utilizes both IL-4Rα/Jak2/Stat3 and IL-13Rα1/Tyk2/Stat1/Stat6 signaling pathways, IL-4 can use only the IL-4Rα/Jak1/Stat3/Stat6 cascade to regulate the expression of some critical inflammatory genes, including 15-lipoxygenase, monoamine oxidase A (MAO-A), and the scavenger receptor CD36. Moreover, we demonstrate here that IL-13 and IL-4 can uniquely affect the expression of particular genes such as dual-specificity phosphatase 1 and tissue inhibitor of metalloprotease-3 and do so through different Jaks. As evidence of differential regulation of gene function by IL-4 and IL-13, we further report that MAO-A-mediated reactive oxygen species generation is influenced by different Jaks. Collectively, these results have major implications for understanding the mechanism and function of alternatively activated monocytes/macrophages by IL-4 and IL-13 and add novel insights into the pathogenesis and potential treatment of various inflammatory diseases.
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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.