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P2Y6 Deficiency Enhances Dendritic Cell–Mediated Th1/Th17 Differentiation and Aggravates Experimental Autoimmune Encephalomyelitis
The Journal of Immunology ( IF 4.4 ) Pub Date : 2020-06-17 , DOI: 10.4049/jimmunol.1900916
Zhenlong Li 1 , Cong He 1 , Jiang Zhang 1 , Hongmei Zhang 1 , Huan Wei 1 , Shijia Wu 1 , Wenzheng Jiang 2
Affiliation  

Key Points P2Y6 deficiency enhances DC-mediated Th1/Th17 differentiation. P2Y6 deficiency aggravates the pathogenesis of EAE. Dendritic cells (DCs) are essential APCs and play a crucial role in initiating and regulating the adaptive immune response. In this study, we have reported that P2Y6, a member of G protein–coupled receptors, inhibits the maturation and activation of DCs via suppressing the activation of the transcription factor NF-κB. Furthermore, loss of P2Y6 does not impact T cells homeostasis in the steady-state. However, in vitro studies show that P2Y6 signaling inhibits the production of IL-12 and IL-23 and the polarization of Th1 and Th17 subsets mediated by DCs. In addition, we find that mice lacking P2Y6 develop more severe experimental autoimmune encephalomyelitis compared with wild-type mice. Our results indicate that P2Y6 functions as a pivotal regulator on DC maturation, and the loss of P2Y6 results in the aggravated experimental autoimmune encephalomyelitis, which suggests that P2Y6 may play a pivotal role in the pathogenesis of autoimmune diseases.

中文翻译:

P2Y6 缺乏增强树突状细胞介导的 Th1/Th17 分化并加重实验性自身免疫性脑脊髓炎

关键点 P2Y6 缺乏增强 DC 介导的 Th1/Th17 分化。P2Y6 缺乏会加重 EAE 的发病机制。树突状细胞 (DC) 是必不可少的 APC,在启动和调节适应性免疫反应中起着至关重要的作用。在这项研究中,我们报道了 G 蛋白偶联受体的成员 P2Y6 通过抑制转录因子 NF-κB 的激活来抑制 DC 的成熟和激活。此外,P2Y6 的缺失不会影响稳态中的 T 细胞稳态。然而,体外研究表明 P2Y6 信号抑制了 IL-12 和 IL-23 的产生以及由 DC 介导的 Th1 和 Th17 亚群的极化。此外,我们发现与野生型小鼠相比,缺乏 P2Y6 的小鼠会发生更严重的实验性自身免疫性脑脊髓炎。
更新日期:2020-06-17
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