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外泌体靶向 HBV-宿主相互作用重塑肝脏免疫微环境。

Exosomes target HBV-host interactions to remodel the hepatic immune microenvironment.

机构信息

Department of Hepatology, Center of Infectious Diseases and Pathogen Biology, The First Hospital of Jilin University, Changchun, Jilin, 130021, People's Republic of China.

出版信息

J Nanobiotechnology. 2024 Jun 5;22(1):315. doi: 10.1186/s12951-024-02544-y.

DOI:10.1186/s12951-024-02544-y
PMID:38840207
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC11151510/
Abstract

Chronic hepatitis B poses a significant global burden, modulating immune cells, leading to chronic inflammation and long-term damage. Due to its hepatotropism, the hepatitis B virus (HBV) cannot infect other cells. The mechanisms underlying the intercellular communication among different liver cells in HBV-infected individuals and the immune microenvironment imbalance remain elusive. Exosomes, as important intercellular communication and cargo transportation tools between HBV-infected hepatocytes and immune cells, have been shown to assist in HBV cargo transportation and regulate the immune microenvironment. However, the role of exosomes in hepatitis B has only gradually received attention in recent years. Minimal literature has systematically elaborated on the role of exosomes in reshaping the immune microenvironment of the liver. This review unfolds sequentially based on the biological processes of exosomes: exosomes' biogenesis, release, transport, uptake by recipient cells, and their impact on recipient cells. We delineate how HBV influences the biogenesis of exosomes, utilizing exosomal covert transmission, and reshapes the hepatic immune microenvironment. And based on the characteristics and functions of exosomes, potential applications of exosomes in hepatitis B are summarized and predicted.

摘要

慢性乙型肝炎在全球造成了巨大负担,其通过调节免疫细胞,导致慢性炎症和长期损伤。由于乙型肝炎病毒(HBV)具有嗜肝性,它不能感染其他细胞。HBV 感染者不同肝内细胞之间的细胞间通讯以及免疫微环境失衡的机制仍不清楚。外泌体作为 HBV 感染的肝细胞与免疫细胞之间重要的细胞间通讯和货物运输工具,已被证明有助于 HBV 货物运输和调节免疫微环境。然而,外泌体在乙型肝炎中的作用近年来才逐渐受到关注。很少有文献系统阐述了外泌体在重塑肝脏免疫微环境中的作用。本综述按照外泌体的生物学过程依次展开:外泌体的发生、释放、运输、被受体细胞摄取,以及它们对受体细胞的影响。我们描述了 HBV 如何影响外泌体的发生,利用外泌体的隐蔽性传递,并重塑肝脏免疫微环境。并且基于外泌体的特点和功能,总结和预测了外泌体在乙型肝炎中的潜在应用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4dff/11151510/2ac9cf5a6c0b/12951_2024_2544_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4dff/11151510/4a5d581e5667/12951_2024_2544_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4dff/11151510/9ccc3608988a/12951_2024_2544_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4dff/11151510/99ffc696e017/12951_2024_2544_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4dff/11151510/2ac9cf5a6c0b/12951_2024_2544_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4dff/11151510/4a5d581e5667/12951_2024_2544_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4dff/11151510/9ccc3608988a/12951_2024_2544_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4dff/11151510/99ffc696e017/12951_2024_2544_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/4dff/11151510/2ac9cf5a6c0b/12951_2024_2544_Fig4_HTML.jpg

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本文引用的文献

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HBV-miR-3 is closely related to HBV replication and strongly predictive of HBeAg seroconversion in PegIFN-α treated patients.HBV-miR-3 与 HBV 复制密切相关,并且在 PegIFN-α 治疗的患者中对 HBeAg 血清学转换具有很强的预测性。
Sci Rep. 2024 Jan 17;14(1):1502. doi: 10.1038/s41598-024-52060-0.
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MDSCs-derived GPR84 induces CD8 T-cell senescence via p53 activation to suppress the antitumor response.
细胞外囊泡在代谢功能障碍相关脂肪性肝病及其他肝脏疾病发病机制中的作用
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Hepatitis B virus entry, assembly, and egress.乙型肝炎病毒的进入、组装和释放。
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髓系来源的 GPR84 通过激活 p53 诱导 CD8 T 细胞衰老,从而抑制抗肿瘤反应。
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Engineered extracellular vesicles for delivering functional Cas9/gRNA to eliminate hepatitis B virus cccDNA and integration.工程化细胞外囊泡递送功能性 Cas9/gRNA 以消除乙型肝炎病毒 cccDNA 和整合。
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