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rFIP-nha通过AIM2炎症酶调节来激活巨细胞,使其转向一种亲炎症的表型

Yusi Liu^1,2,3, Zhen Li³, Harry Wichers^1,2

¹Wageningen Food and Biobased Research, Wageningen University and Research, Wageningen, Netherlands.

Frontiers in cell and developmental biology

|May 13, 2025

概括

性免疫调节蛋白FIP-nha激活巨细胞,诱导诸如IL-1β之类的促炎细胞因子. 这独立于糖化,通过AIM2炎症酶途径发生,揭示了真菌蛋白免疫调节的新机制.

科学领域:

菌类学菌类学是指菌类学.
免疫学免疫学免疫学
分子生物学分子生物学

背景情况:

真菌免疫调节蛋白 (FIP) 具有显著的免疫调节作用.
来自Nectria haematococca的FIP-nha显示出热稳定性和抗瘤活性,但其巨细胞相互作用机制尚不清楚.
在FIP-nha中的糖化位可能会影响其生物功能.

研究的目的:

研究FIP-nha对巨细胞的免疫调节活性.
阐明FIP-nha诱导的巨细胞激活背后的机制.
确定糖化在FIP-nha的免疫调节功能中的作用.

主要方法:

在Pichia pastoris*中,FIP-nha甘氨酸突变体 (N5A,N39A,N5+39A) 的重组表达.
评估THP-1巨细胞化,细胞因子分泌 (IL-1β,IL-12,IL-10) 和基因表达.
使用THP1-KO-ASC细胞和抑制剂,分析炎症酶 (NLRP1,NLRP3,NLRC4,AIM2) 激活和对ASC信号通路的依赖.

主要成果:

再组合的FIP-nha及其甘氨酸突变物减少了巨细胞化,但显著诱导了前炎性细胞因子分泌 (IL-1β,IL-12,IL-10).
野生类型FIP-nha与其甘氨酸突变体之间没有观察到免疫调节活性的显著差异,这表明了独立于糖化酶的机制.
FIP-nha显著提高了AIM2炎症体转录的调节,IL-1β的释放取决于ASC信号通路.

结论:

FIP-nha激活了THP-1巨细胞,促进了促炎反应.
FIP-nha的免疫调节活性独立于其糖化.
FIP-nha通过AIM2炎症体和ASC信号通路激活巨细胞.

关键词:

在AIM2炎症酶中,有AIM2炎症酶.一个IL-1ββ.葡萄糖酶化是什么? 葡萄糖酶化是什么?免疫调节蛋白质是一种免疫调节蛋白.巨细胞是一个巨细胞.它们是促炎性炎症.

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