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在狼性炎中,S1P/S1PR1轴通过NLRP3炎症酶激活促进巨细胞M1两极化

Jihua Tian¹, Sijia Chang¹, Jing Wang¹

¹Department of Microbiology and Immunology, Shanxi Medical University, Taiyuan, Shanxi, China.

Molecular immunology

|June 28, 2023

概括

升高的基-1-酸盐 (S1P) 驱动狼性炎 (LN),通过通过S1PR1和NLRP3炎症酶激活促进M1巨细胞的积累. 在狼小鼠模型中,用FTY720阻断S1PR1改善了炎.

科学领域:

免疫学免疫学免疫学
腎臟病學 (nephrology) 是一種醫學專業.
药理学药理学是指药理学的学科.

背景情况:

狼性炎 (LN),系统性红斑狼 (SLE) 的严重并发症,是死亡的主要原因.
在SLE患者和狼模型中观察到高基-1-酸盐 (S1P) 水平,FTY720显示治疗潜力.
在LN的巨细胞介导炎中S1P信号的作用仍然在很大程度上未被探索.

研究的目的:

调查S1P及其受体在狼性炎病变发生过程中的作用.
在LN的背景下探索S1P和巨细胞之间的相互作用.
确定针对狼性炎中S1P途径的治疗潜力.

主要方法:

在MRL/lpr狼小鼠模型中分析S1P水平和S1PR1表达.
用FTY720阻止S1PR1并评估炎的改善.
实验室内研究,以检查S1P对巨分极和NLRP3炎症酶激活的影响.

主要成果:

在MRL/lpr小鼠中,S1P水平和S1PR1表达升高.
在MRL/lpr小鼠中,FTY720治疗显著改善了炎症状.
升高的S1P促进了M1型巨细胞的积累,S1P/S1PR1激活通过NLRP3炎症体诱导了M1极化.

结论:

巨细胞S1PR1在狼性炎的发病过程中发挥着关键作用.
该S1P/S1PR1通路促进M1巨细胞两极化和脏炎症在LN.
针对S1P信号提供了一种新的治疗策略,用于狼性炎.

关键词:

狼性炎是一种神经炎.巨细胞的两极分化含有3个pyrin域的NLR家族的3个pyrin域.斯芬哥辛-1-酸盐是一种酸盐.斯芬哥辛-1-酸盐受体的受体

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