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在牙周炎中,PGRN通过TNFR2参与巨细胞M2极化调节

Liguo Zhang¹, Fujiao Nie¹, Jingjing Zhao¹

¹Department of Periodontology, School and Hospital of Stomatology, Cheeloo College of Medicine, Shandong Key Laboratory of Oral Tissue Regeneration & Shandong Engineering Laboratory for Dental Materials and Oral Tissue Regeneration & Shandong Provincial Clinical Research Center for Oral Diseases, Shandong University, Jinan, Shandong, 250012, China.

Journal of translational medicine

|April 30, 2024

概括

前列腺素 (PGRN) 通过与TNFR2.2结合,促进牙周炎中M2巨分化. 这一发现澄清了PGRN在牙周病中的免疫作用,影响炎症和组织修复.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
牙周病学牙周病学

背景情况:

进子素 (PGRN) 是一种生长因子,已知在各种疾病中起作用.
它在牙周炎中的特定免疫调节功能,特别是关于巨细胞两极分化,仍然不清楚.

研究的目的:

调查PGRN对牙周炎微环境中的巨细胞两极分化的调节作用.
阐明潜在的分子机制,包括TNFR2.2的作用.

主要方法:

在人类牙样本上的免疫组织化学 (IHC) 和多重IHC.
在体外研究使用RAW264.7细胞和骨髓衍生巨细胞 (BMDMs) 用LPS或IL-4刺激,有或没有PGRN.
基因和蛋白质表达分析 (qRT-PCR,IF,ELISA,流细胞计).
同免疫沉和TNFR2阻断试验.

主要成果:

大细胞积聚在牙周炎组织中,M1和M2标记物增加. PGRN表达升高,并与M2巨细胞共同定位.
在LPS刺激的巨细胞中,PGRN治疗降低了M1标记物,增加了M2标记物.
PGRN增强了IL-4诱导的M2极化,并与TNFR2.2直接相互作用.
TNFR2封锁取消了PGRN对M2极化的影响.

结论:

进子素 (PGRN) 在牙周炎中促进M2巨分化.
这种效应是通过PGRN与其受体TNFR2.2的结合来实现的.
在促炎和抗炎性牙周疾病中,PGRN会影响巨细胞表型.

关键词:

巨细胞的两极分化多重光免疫组织化学学在PGRNN中使用.牙周病是指牙周病的发生.这就是TNFR2的特点.

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