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CXCL4和CXCL4L1通过TLR4信号来激活人类巨细胞,以调节炎症反应

Han Bai^1,2, Ruoxi Yuan³, Dong Yan⁴

¹Department of Blood Transfusion, The First Affiliated Hospital of Xi'an Jiaotong University, 277 Yanta West Road, Yanta District, Xi'an 710061, Shaanxi, China.

|December 24, 2025

概括

化学物质CXCL4通过托尔类受体4 (TLR4) 激活单细胞,导致炎症和亡. 用CXCL4L1准TLR4在喘模型中显示了治疗潜力.

科学领域:

免疫学免疫学免疫学
细胞生物学细胞生物学
分子医学是分子医学.

背景情况:

化学物质CXCL4 (CXCL4) 有助于炎症和纤维性疾病.
人体单细胞/巨细胞中缺少CXCL4的受体CXCR3,因此其信号通路尚不清楚.

研究的目的:

阐明信号通路和受体调解人类单细胞/巨细胞对CXCL4的反应.
研究托尔类受体4 (TLR4) 在CXCL4诱导的细胞反应和疾病发病过程中的作用.

主要方法:

使用了人类初级单细胞和来自小鼠骨髓的巨细胞.
分析了NF-κB,TBK1-JNK-AP1和TRIF-RIPK3的信号轴.
研究CXCL4/CXCL4L1与TLR4/MD-2复合物的相互作用.
在小鼠喘模型中,用于异位CXCL4L1表达的腺相关病毒 (AAV).
在野生型和TLR4缺乏的小鼠中比较反应.

主要成果:

CXCL4激活了NF-κB和TBK1-JNK-AP1轴,诱导炎症,纤维化和化学基因基因表达.
在人体单细胞中,CXCL4触发了TRIF-RIPK3轴依赖性亡.
CXCL4和CXCL4L1与TLR4/MD-2复合体相互作用,CXCL4L1诱导了与LPS不同的转录组形状.
异位CXCL4L1表达在野生型小鼠中减轻了喘,但在TLr4缺乏的小鼠中没有.

结论:

CXCL4及其变体CXCL4L1调节人类单细胞中的炎症和纤维化的基因表达和亡.
CXCL4/CXCL4L1通过TLR4依赖信号调节肺炎.
在对CXCL4/CXCL4L1.1.的病理生理反应中,TLR4起着至关重要的作用.

关键词:

喘喘是一种在CXCL4中,CXCL4是CXCL4.在CXCL4L1中,尸体灭 (Necroptosis) 是一种死亡的过程.在 TLR4 中,

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