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在心脏移植拒绝过程中通过PCSK9/CD36途径对肝脏进行免疫调节

Xi Zhang^1,2, Heng Xu¹, Jizhang Yu^1,2

¹Department of Cardiovascular Surgery (X.Z., H.X., J.Y., J.C., Z.C., Y.L., Y.N., S.W., S.R., Y.Z., J.W., J.X.), Union Hospital, Tongji Medical College, Huazhong University of Science and Technology, Wuhan, China.

|May 26, 2023

概括

在心脏移植排斥 (HTR) 期间高PCSK9水平会促进炎症. 通过调节CD36通路,阻断PCSK9 (proprotein转化酶亚素/ kexin 9) 可能通过调节巨细胞功能来防止HTR.

科学领域:

免疫学
肝病学
心血管科学

背景情况:

蛋白转化酶亚素/ 素9 (PCSK9) 是肝脏分泌的蛋白质,用于高脂血症和心血管疾病.
已知PCSK9在免疫调节中的作用,但其在心脏移植排斥 (HTR) 中的作用尚不清楚.

研究的目的:

研究PCSK9和肝脏在HTR中的作用.
阐明HTR中PCSK9介导的免疫调节的潜在机制.

主要方法:

在小鼠和人类HTR模型中评估血清PCSK9水平.
使用PCSK9淘汰小鼠和中和抗体来研究PCSK9剥离效应.
进行多器官组织学,转录组,多组学和单细胞RNA测序分析.
研究了PCSK9/CD36通路对巨细胞表型和功能的影响.

主要成果:

在HTR期间,在小鼠和人类接受者中观察到血清PCSK9水平升高.
切除PCSK9延长了心脏移植的存活时间,并减少了炎症细胞的透.
肝脏被确定为HTR期间受TNF-α和IFN-γ影响的PCSK9上调的主要来源.
PCSK9抑制了巨细胞的CD36表达,并促进了亲炎性表型,增强了T细胞的反应.

结论:

肝脏通过PCSK9/CD36途径调节HTR,影响巨细胞的功能.
向PCSK9/CD36通路是预防HTR的潜在治疗策略.

关键词:

CD36抗原 PCSK9 抑制剂的使用所有移植心脏移植肝细胞脂质新陈代谢肝脏巨细胞

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