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骨肝相互作用通过Pinch-Cxcl12-Mbl2通路调节免疫和造血功能

Tailin He¹, Bo Zhou¹, Guohuan Sun²

¹Department of Biochemistry, School of Medicine, Southern University of Science and Technology, Guangdong Provincial Key Laboratory of Cell Microenvironment and Disease Research, Shenzhen Key Laboratory of Cell Microenvironment, Shenzhen, 518055, China.

Cell death and differentiation

|December 7, 2023

概括

缺少Pinch1/2蛋白质的介酶体 stromal 细胞 (MSCs) 会损害免疫功能和造血. 在小鼠中恢复Mbl2蛋白水平,从而拯救了免疫缺陷,揭示了一条新的治疗途径.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
分子生物学分子生物学

背景情况:

介质细胞 stromal 细胞 (MSCs) 用于治疗免疫和传染病,但其精确的机制尚未完全理解.
辛奇蛋白在MSC功能中的作用及其对免疫调节的影响需要进一步阐明.

研究的目的:

研究Pinch1/2蛋白在骨髓 stromal 细胞 (BMSCs) 中的功能及其在免疫和造血调节中的作用.
为了识别通过Pinch蛋白调节免疫力和血液形成的分子通路.

主要方法:

使用了Prx1-Cre;Pinch1^f/f;Pinch2^-/-转基因小鼠来研究BMSC中Pinch缺乏症的影响.
采用单细胞测序来分析BMSC亚群和造血细胞分化.
使用脂聚糖 (LPS) 诱导的急性肺损伤和硫酸 (DSS) 诱导的炎症性肠病模型评估炎症反应.
研究了Cxcl12在BMSC和Mbl2补充在肝细胞中的表达.

主要成果:

在BMSC中缺乏Pinch1/2蛋白质的小鼠表现出严重的免疫和造血缺陷,导致过早死亡.
在BMSC中缩缺陷损害了造血细胞的成熟,增加了单细胞中促炎性细胞因子 (TNF-α,IL-1β) 的产生.
失去Pinch降低了BMSC中的Cxcl12表达,随后降低了肝细胞中的Mbl2补充,并降低了先天免疫力.
在小鼠中,给予重组Mbl2蛋白挽救了皮奇缺乏BMSCs的致死性.

结论:

ピン奇-Cxcl12-Mbl2信号通路通过调节骨肝相互作用来调节免疫和血液形成至关重要.
针对这种途径为免疫和传染病提供了潜在的治疗策略.

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