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格林激活TNFR2促进巨细胞M2极化恶化菌根结核病感染

Bingling Zhang¹, Lan Xiang², Jun Chen²

¹Disease Control and Prevention, Zhangqiao Branch, Ningbo Ninth Hospital Medical Health Group, 315000 Ningbo, Zhejiang, China.

Frontiers in bioscience (Landmark edition)

|September 30, 2024

概括

颗粒素 (GRN) 通过上调瘤亡因子受体2 (TNFR2) 表达来促进结核病中的M2巨细胞两极化. 这一发现澄清了Mtb感染的机制,并提出了潜在的治疗点.

科学领域:

免疫学免疫学免疫学
传染性疾病传染性疾病
细胞生物学细胞生物学

背景情况:

巨细胞两极分化在传染病中至关重要,M2两极分化在病理学上具有重要意义.
在Mycobacterium结核病 (Mtb) 感染中M2极化机制尚未完全理解.
在M2极化中,花素 (GRN) 和瘤亡因子受体2 (TNFR2) 的作用需要进一步研究.

研究的目的:

为了研究M2巨分化对Mtb感染的影响.
阐明GRN和TNFR2影响M2偏振的机制.

主要方法:

量化RT-PCR和流细胞计用于分析肺结核 (PTB) 患者和健康对照者的GRN和TNFR2水平和巨细胞表型.
在体外研究中,IL-4用于诱导RAW264.7细胞的M2两极化,随后是GRN淘汰和/或TNFR2过度表达.
使用Western Blot,RT-qPCR,免疫光和免疫沉来评估标记物表达,蛋白质结合和功能影响.

主要成果:

与健康个体相比,PTB患者表现出高GRN和TNFR2表达,M2巨细胞占主导地位.
GRN的淘汰将巨细胞的两极分化转向M1,减少M2标记物和增加M1标记物.
发现GRN与TNFR2结合,并对其表达进行上调,从而促进M2极化.

结论:

在PTB患者中,GRN和TNFR2的表达高.
通过增强TNFR2表达,GRN促进M2巨细胞的两极分化,从而提供了对Mtb病变的洞察力.

关键词:

在M2中,极化为M2.结核病菌菌菌的结核病菌的结核病菌.这就是TNFR2的特点.这种蛋白质叫做granulin.巨细胞是什么?巨细胞是什么?结核病是一种肺结核病.

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