IL-33-activated murine mast cells control the dichotomy between RORγt + and Helios + T regs via the MK2/3-mediated IL-6 production in vitro.

Autor: Andreas N; Institut für Immunologie, Universitätsklinikum Jena, Jena, Germany., Weber F; Institut für Immunologie, Universitätsklinikum Jena, Jena, Germany., Meininger I; Institut für Immunologie, Universitätsklinikum Jena, Jena, Germany., Templin N; Institut für Immunologie, Universitätsklinikum Jena, Jena, Germany., Gaestel M; Institut für Zellbiochemie, Medizinische Hochschule Hannover, Hannover, Germany., Kamradt T; Institut für Immunologie, Universitätsklinikum Jena, Jena, Germany., Drube S; Institut für Immunologie, Universitätsklinikum Jena, Jena, Germany.
Jazyk: angličtina
Zdroj: European journal of immunology [Eur J Immunol] 2019 Dec; Vol. 49 (12), pp. 2159-2171. Date of Electronic Publication: 2019 Jul 30.
DOI: 10.1002/eji.201948154
Abstrakt: In mast cells, IL-33 typically induces the activation of NF-κB, which results in the production of cytokines such as IL-6 and IL-2. Here, we demonstrate that the IL-33-induced IL-6 production in murine mast cells and the formation of RORγt + T regs essentially depends on the MAPKAPs, MK2, and MK3 (MK2/3) downstream of MyD88. In contrast to this, the IL-33-induced and MyD88-dependent IL-2 production in mast cells contributes to the maintenance of Helios + T regs . Thereby, the IL-33-induced IL-2 response and, thus, the maintenance of Helios + T regs are limited by an IL-6-mediated autocrine negative feedback stimulation acting on mast cells. Collectively, we present MK2/3 in IL-33-activated mast cells as a signaling node, which controls the dichotomy between RORγt + T reg and Helios + T reg in vitro.
(© 2019 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim.)
Databáze: MEDLINE
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