ArticleScientific reports2020
The IL-33-induced p38-/JNK1/2-TNFα axis is antagonized by activation of β-adrenergic-receptors in dendritic cells.
Article in Scientific reports, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed, 15 citations in OpenAlex.
- Targeting JNK1/2 and P38 Mitogen-Activated Protein Kinases With Pazopanib Mitigates Bleomycin-Induced Lung Fibrosis.Archiv der Pharmazie · 2025Article
- IL-33/ST2 axis of human amnion fibroblasts participates in inflammatory reactions at parturition.Molecular medicine (Cambridge, Mass.) · 2023Article
- Identification of novel candidate targets for suppressing ovarian cancer progression through IL-33/ST2 axis components using the system biology approach.Frontiers in molecular biosciences · 2023Article
- EnterotoxigenicInfection and immunity · 2022Article
- Fast Maturation of Splenic Dendritic Cells Upon TBI Is Associated With FLT3/FLT3L Signaling.Frontiers in immunology · 2022Article
- The p38Frontiers in cell and developmental biology · 2021Review
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Authors and funding
7 authors at 2 institutions in 1 country.
Funding
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Abstract
IL-33, an IL-1 cytokine superfamily member, induces the activation of the canonical NF-κB signaling, and of Mitogen Activated Protein Kinases (MAPKs). In dendritic cells (DCs) IL-33 induces the production of IL-6, IL-13 and TNFα. Thereby, the production of IL-6 depends on RelA whereas the production of IL-13 depends on the p38-MK2/3 signaling module. Here, we show that in addition to p65 and the p38-MK2/3 signaling module, JNK1/2 are essential for the IL-33-induced TNFα production. The central roles of JNK1/2 and p38 in DCs are underpinned by the fact that these two MAPK pathways are controlled by activated β-adrenergic receptors resulting in a selective regulation of the IL-33-induced TNFα response in DCs.
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