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长期的高血糖症对M1-和M2-类巨细胞有截然不同的影响

Sona Margaryan¹, David Poghosyan¹, Susanna Ghonyan¹

¹Laboratory of Molecular and Cellular Immunology, Institute of Molecular Biology, National Academy of Sciences, Yerevan, Armenia.

Frontiers in immunology

|August 18, 2025

概括

慢性高血糖会损害巨细胞的功能. 高葡萄糖将M2巨细胞转移到M1上,破坏免疫反应,并可能解释代谢障碍中的巨细胞两极分化.

科学领域:

免疫学免疫学免疫学
代谢障碍代谢障碍代谢障碍
细胞生物学细胞生物学

背景情况:

慢性高血糖是代谢障碍的标志,破坏细胞平衡和免疫功能.
巨细胞,关键的先天性免疫细胞,具有适应性,并利用葡萄糖作为能量.
独特的M1 (前炎性) 和M2 (修复性) 巨细胞表型在免疫中起着至关重要的作用.

研究的目的:

为了研究高血糖在M1和M2巨细胞两极分化和功能的体外影响.
确定高葡萄糖状况如何改变M1和M2巨细胞在炎症反应中的独特作用.

主要方法:

初级单细胞分化为M1和M2类巨细胞.
用一个体外高血糖模型来模拟慢性高血糖状况.
功能性测试评估了反应性氧物种 (ROS) 生产,细胞因子分泌 (IL-6,TNF-α),抗原呈现,共刺激分子表达 (CD86,HLA-DR),细胞能力和内毒素耐受性.

主要成果:

高血糖症降低了M1巨细胞的功能,降低了ROS的产生,IL-6和TNF-α的分泌,抗原呈现和协同刺激能力.
暴露于高血糖的M2巨细胞向M1极化转移,ROS和IL-6的产生增加,CD86和HLA-DR的表达增加,修复功能受损.
内毒素耐受性受到干扰,由TNF-α的产生增加和在高血糖条件下M2巨细胞的细胞能力降低所证明.

结论:

慢性高血糖症破坏了M1和M2巨细胞的功能专业化,模糊了它们不同的作用.
这些发现表明,高血糖引起的巨细胞失调可能会导致代谢综合征患者组织巨细胞中观察到的混合两极化.

关键词:

转基因CSF和M-CSF衍生的细胞在LPS中使用LPS.M1 和 M2 巨细胞.耐受性耐受性内毒素耐受性过高血糖症是什么意思发酵细胞的形成发酵细胞的形成

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