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The IL-33-induced p38-/JNK1/2-TNF? axis is antagonized by activation of ?-adrenergic-receptors in dendritic cells.


ABSTRACT: IL-33, an IL-1 cytokine superfamily member, induces the activation of the canonical NF-?B signaling, and of Mitogen Activated Protein Kinases (MAPKs). In dendritic cells (DCs) IL-33 induces the production of IL-6, IL-13 and TNF?. 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 TNF? 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 ?-adrenergic receptors resulting in a selective regulation of the IL-33-induced TNF? response in DCs.

SUBMITTER: Helbig C 

PROVIDER: S-EPMC7235212 | biostudies-literature | 2020 May

REPOSITORIES: biostudies-literature

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The IL-33-induced p38-/JNK1/2-TNFα axis is antagonized by activation of β-adrenergic-receptors in dendritic cells.

Helbig Christiane C   Weber Franziska F   Andreas Nico N   Herdegen Thomas T   Gaestel Matthias M   Kamradt Thomas T   Drube Sebastian S  

Scientific reports 20200518 1


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 r  ...[more]

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