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在炎症刺激过程中,LAMP1控制CXCL10-CXCR3轴介导的巨细胞两极分化的炎症调节

Yingying Ye¹, Lexing Li², Hu Kang³

¹Department of Biochemistry and Molecular Biology, School of Laboratory Medicine, and Anhui Province Key Laboratory of Cancer Translational Medicine, Bengbu Medical University, 2600 Donghai Avenue, Bengbu, Anhui 233030, China; Reproduction Medicine Center, The First Affiliated Hospital of Bengbu Medical University, Bengbu, Anhui, 233030, China.

International immunopharmacology

|March 31, 2024

概括

CXCL10-CXCR3轴影响巨细胞的两极分化,其中自细胞蛋白LAMP1作为关键开关. 这个轴在炎症和非炎症状态下差异地引导巨细胞两极分化,影响肺损伤.

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:

CXCL10-CXCR3轴与炎症反应有关.
巨细胞极化和自在炎症中至关重要,但它们与巨细胞中CXCL10-CXCR3轴的相互作用尚不清楚.

研究的目的:

调查CXCL10-CXCR3轴在通过自性调节巨细胞极化中的作用.
阐明在这个过程中自蛋白的特定功能.

主要方法:

在非炎症性和多I:C刺激的炎症性巨细胞中对CXCL10和CXCR3抗剂AMG487的反应中检查了巨细胞极化 (M1/M2).
评估了关键的自蛋白 (Atg5-Atg12,p62,LC3-II,LAMP1) 的表达.
利用短干扰RNA (siRNA) 来敲击LAMP1并评估其对巨细胞两极分化的影响.
研究了AMG487的治疗潜力,在一个由多种I:C诱导的肺损伤的小鼠模型中.

主要成果:

在非炎症性巨细胞中,CXCL10促进了M2极化,而AMG487诱导了M1极化. CXCL10增加了自蛋白的表达,而AMG487降低了它.
在非炎症性巨细胞中,LAMP1的抑制逆转了CXCL10诱导的M2偏向到M1.
在炎症性巨细胞中,CXCL10诱导M1两极化,AMG487诱导M2两极化,LAMP1表达减少.
治疗AMG487缓解了小鼠的肺损伤后的多种I:C) 管理.

结论:

CXCL10-CXCR3轴在炎症和非炎症条件下差异调节巨细胞两极分化.
自蛋白LAMP1作为一个关键开关,指导由CXCL10-CXCR3轴介导的极化结果.
准CXCL10-CXCR3轴可能为炎症性肺部疾病提供治疗益处.

关键词:

自自是一种自的过程.在CXCR3受体中,CXCR3受体是炎症炎症是一种炎症.巨细胞的两极分化

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