IL-33-activated murine mast cells control the dichotomy between RORγt+ and Helios+ Tregs via the MK2/3-mediated IL-6 production in vitro.,European Journal of Immunology

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IL-33-activated murine mast cells control the dichotomy between RORγt+ and Helios+ Tregs via the MK2/3-mediated IL-6 production in vitro.
European Journal of Immunology ( IF 4.5 ) Pub Date : 2019-07-30 , DOI: 10.1002/eji.201948154
Nico Andreas ₁ , Franziska Weber ₁ , Isabel Meininger ₁ , Nicole Templin ₁ , Matthias Gaestel ₂ , Thomas Kamradt ₁ , Sebastian Drube ₁

Affiliation

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+ Tregs 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+ Tregs . Thereby, the IL-33-induced IL-2 response and, thus, the maintenance of Helios+ Tregs 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+ Treg and Helios+ Treg in vitro.

中文翻译：

IL-33激活的小鼠肥大细胞通过MK2 / 3介导的IL-6体外生产来控制RORγt+和Helios + Treg之间的二分法。

在肥大细胞中，IL-33通常会诱导NF-κB活化，从而导致细胞因子（如IL-6和IL-2）的产生。在这里，我们证明了小鼠肥大细胞中IL-33诱导的IL-6产生以及RORγt+ Treg的形成基本上取决于MyD88下游的MAPKAP，MK2和MK3（MK2 / 3）。与此相反，肥大细胞中由IL-33诱导和依赖MyD88的IL-2产生有助于维持Helios + Treg。因此，IL-33诱导的IL-2反应以及因此Helios + Treg的维持受到作用于肥大细胞的IL-6介导的自分泌负反馈刺激的限制。总的来说，我们目前在IL-33激活的肥大细胞中将MK2 / 3作为信号转导节点，在体外控制RORγt+ Treg和Helios + Treg之间的二分法。

更新日期：2019-07-30

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