| First Author | Helbig C | Year | 2020 |
| Journal | Sci Rep | Volume | 10 |
| Issue | 1 | Pages | 8152 |
| PubMed ID | 32424229 | Mgi Jnum | J:298448 |
| Mgi Id | MGI:6480129 | Doi | 10.1038/s41598-020-65072-3 |
| Citation | Helbig C, et al. (2020) The IL-33-induced p38-/JNK1/2-TNFalpha axis is antagonized by activation of beta-adrenergic-receptors in dendritic cells. Sci Rep 10(1):8152 |
| abstractText | IL-33, an IL-1 cytokine superfamily member, induces the activation of the canonical NF-kappaB signaling, and of Mitogen Activated Protein Kinases (MAPKs). In dendritic cells (DCs) IL-33 induces the production of IL-6, IL-13 and TNFalpha. 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 TNFalpha 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 beta-adrenergic receptors resulting in a selective regulation of the IL-33-induced TNFalpha response in DCs. |
