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在健康个体和心力衰竭患者中,中性粒细胞中CD41/CD61复合物的表达均有助于其黏附性。

Neutrophil expression of CD41/CD61 complex contributes to their adhesiveness in both healthy individuals and heart failure patients.

作者信息

Djouani Melissa, Dumont Benjamin L, Neagoe Paul-Eduard, Villeneuve Louis, Tardif Jean-Claude, Gagnon Daniel, Racine Normand, White Michel, Sirois Martin G

机构信息

Research center, Montreal Heart Institute, 5000 Belanger Street, Montreal, Qc, H1T 1C8, Canada.

Department of pharmacology and physiology, Université de Montréal, Montreal, Qc, Canada.

出版信息

BMC Immunol. 2025 Aug 30;26(1):63. doi: 10.1186/s12865-025-00742-3.


DOI:10.1186/s12865-025-00742-3
PMID:40885916
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC12398050/
Abstract

BACKGROUND: Neutrophils can release pro-inflammatory cytokines and neutrophil extracellular traps (NETs), leading to vascular thrombosis. Neutrophil-platelet interaction, a major component of thrombosis, is more pronounced in inflammatory pathologies, such as heart failure (HF). Recently, the platelet receptor CD41/CD61 (GPIIb/IIIa), known for its role in platelet adhesion and aggregation via its binding to fibrinogen, was found on the membrane of neutrophils from lung cancer patients. Our objectives were to determine CD41/CD61 expression on neutrophils and its role in healthy volunteers (HV) and acute decompensated heart failure patients (ADHF). RESULTS: Localization and expression of CD41/CD61 complex on isolated neutrophils were determined by flow cytometry and confocal microscopy. We assessed the CD41/CD61 role on neutrophil adhesion onto human extracellular matrix (hECM), NETosis and release of inflammatory cytokines. CD41/CD61 complex was intracellularly expressed in 80–90% of neutrophils, but only between 8 and 13% on their extracellular membrane. The CD41/CD61 complex plays a role in neutrophil adhesion onto hECM, since its blockade by an anti-CD41 monoclonal antibody or its antagonist, eptifibatide, reduced CXCL8 and PMA induced neutrophil adhesion from 52 to 100% in both HV and ADHF patients. CONCLUSIONS: In summary, neutrophil specific CD41/CD61 expression contributes to neutrophil adhesiveness without affecting significantly the release of inflammatory cytokines and NETosis in both HV and ADHF patients. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1186/s12865-025-00742-3.

摘要

背景:中性粒细胞可释放促炎细胞因子和中性粒细胞胞外陷阱(NETs),导致血管血栓形成。中性粒细胞与血小板的相互作用是血栓形成的主要组成部分,在诸如心力衰竭(HF)等炎症性疾病中更为明显。最近,血小板受体CD41/CD61(糖蛋白IIb/IIIa),因其通过与纤维蛋白原结合在血小板黏附和聚集中的作用而闻名,在肺癌患者的中性粒细胞膜上被发现。我们的目的是确定健康志愿者(HV)和急性失代偿性心力衰竭患者(ADHF)中性粒细胞上CD41/CD61的表达及其作用。 结果:通过流式细胞术和共聚焦显微镜确定分离的中性粒细胞上CD41/CD61复合物的定位和表达。我们评估了CD41/CD61在中性粒细胞黏附于人细胞外基质(hECM)、NETosis和炎症细胞因子释放中的作用。CD41/CD61复合物在80%-90%的中性粒细胞内表达,但仅在其细胞外膜上的表达介于8%-13%之间。CD41/CD61复合物在中性粒细胞黏附于hECM中起作用,因为抗CD41单克隆抗体或其拮抗剂依替巴肽对其进行阻断后,可使HV和ADHF患者中CXCL8和佛波醇肉豆蔻酸酯乙酸酯(PMA)诱导的中性粒细胞黏附降低52%-100%。 结论:总之,中性粒细胞特异性CD41/CD61表达有助于中性粒细胞黏附性,而在HV和ADHF患者中均未显著影响炎症细胞因子的释放和NETosis。 补充信息:在线版本包含可在10.1186/s12865-025-00742-3获取的补充材料。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fd6/12398050/9ba0b58107aa/12865_2025_742_Fig6_HTML.jpg
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https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fd6/12398050/9ba0b58107aa/12865_2025_742_Fig6_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fd6/12398050/cd512df7e26c/12865_2025_742_Fig1_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fd6/12398050/6b0afa1c2218/12865_2025_742_Fig2_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fd6/12398050/f598b505acad/12865_2025_742_Fig3_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fd6/12398050/918ef3b99d71/12865_2025_742_Fig4_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fd6/12398050/69cb5c344607/12865_2025_742_Fig5_HTML.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/2fd6/12398050/9ba0b58107aa/12865_2025_742_Fig6_HTML.jpg

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本文引用的文献

[1]
Efficacy and safety of toripalimab in the treatment of nasopharyngeal carcinoma: a meta-analysis of single-arm trials.

BMC Immunol. 2025-8-25

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Immunology. 2025-5

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Low-Density Neutrophils and Neutrophil Extracellular Traps (NETs) Are New Inflammatory Players in Heart Failure.

Can J Cardiol. 2024-9

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Invest Ophthalmol Vis Sci. 2023-10-3

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Card Fail Rev. 2023-7-27

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Nat Rev Immunol. 2023-8

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Am J Cardiol. 2022-9-1

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Front Cardiovasc Med. 2022-1-31

[10]
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Blood Adv. 2022-4-12

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