肾纤维化中巨噬细胞活化受EGFR米托贝诱导,其携带的源自小管上皮细胞的MHC-1B外泌体可抑制巨噬细胞活化

Jin Guo , Xuanqi Liu , Haoming Song , Yong Gu , Jianying Niu , Lin Yang
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引用次数: 0

摘要

慢性肾脏疾病(CKD)的高患病率是全球重大的公共卫生负担。肾纤维化是几乎所有CKD病例不可避免的病理过程。迄今为止,预防或延缓肾纤维化进展的可用治疗是有限的。表皮生长因子受体(EGFR)莫托普已被证明可作为一种疫苗减轻单侧输尿管梗阻(UUO)模型中的肾纤维化。进一步的观察表明,EGFR抑制剂可以抑制巨噬细胞的活化,而巨噬细胞在肾纤维化中起重要作用。在当前的研究中,我们探索了EGFR移位在小管上皮细胞(tec)和巨噬细胞之间引发的联系。一系列实验表明,EGFR基因座免疫可以抑制tec衍生外泌体对THP-1巨噬细胞的激活。注射这些外泌体可改善UUO模型的肾纤维化。机制分析表明,主要组织相容性复合体- 1b (MHC-1B)是EGFR免疫诱导tec外泌体的关键分子,受核糖体蛋白L6 (RPL-6)调控。本研究揭示了EGFR mimotope的新的特异性工作途径,提示EGFR mimotope的应用可以扩展到其他免疫相关疾病。
本文章由计算机程序翻译,如有差异,请以英文原文为准。

MHC-1B carried exosomes derived from tubular epithelial cell induced by the EGFR mimotope inhibit macrophage activation in renal fibrosis

MHC-1B carried exosomes derived from tubular epithelial cell induced by the EGFR mimotope inhibit macrophage activation in renal fibrosis
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来源期刊
Extracellular vesicle
Extracellular vesicle Biochemistry, Genetics and Molecular Biology (General)
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