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2
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本文引用的文献

1
The molecular basis of macrophage fusion.巨噬细胞融合的分子基础。
Immunobiology. 2007;212(9-10):785-93. doi: 10.1016/j.imbio.2007.09.012. Epub 2007 Nov 9.
2
Multinucleate giant cells release functionally unopposed matrix metalloproteinase-9 in vitro and in vivo.多核巨细胞在体外和体内释放功能上无拮抗的基质金属蛋白酶-9。
J Infect Dis. 2007 Oct 1;196(7):1076-9. doi: 10.1086/521030. Epub 2007 Aug 20.
3
CD36 signals to the actin cytoskeleton and regulates microglial migration via a p130Cas complex.CD36向肌动蛋白细胞骨架发出信号,并通过p130Cas复合物调节小胶质细胞迁移。
J Biol Chem. 2007 Sep 14;282(37):27392-27401. doi: 10.1074/jbc.M702887200. Epub 2007 Jul 9.
4
Foreign body giant cell formation is preceded by lamellipodia formation and can be attenuated by inhibition of Rac1 activation.异物巨细胞的形成先于片状伪足的形成,并且可以通过抑制Rac1激活而减弱。
Am J Pathol. 2007 Aug;171(2):632-40. doi: 10.2353/ajpath.2007.061213. Epub 2007 Jun 7.
5
Cell-cell fusion.细胞间融合
FEBS Lett. 2007 May 22;581(11):2181-93. doi: 10.1016/j.febslet.2007.03.033. Epub 2007 Mar 21.
6
Macrophage fusion induced by IL-4 alternative activation is a multistage process involving multiple target molecules.由白细胞介素-4诱导的替代性活化巨噬细胞融合是一个涉及多个靶分子的多阶段过程。
Eur J Immunol. 2007 Jan;37(1):33-42. doi: 10.1002/eji.200636788.
7
Oxidized phosphatidylserine-CD36 interactions play an essential role in macrophage-dependent phagocytosis of apoptotic cells.氧化磷脂酰丝氨酸与CD36的相互作用在巨噬细胞依赖性凋亡细胞吞噬过程中起重要作用。
J Exp Med. 2006 Nov 27;203(12):2613-25. doi: 10.1084/jem.20060370. Epub 2006 Nov 13.
8
Scavenger receptors in atherosclerosis: beyond lipid uptake.动脉粥样硬化中的清道夫受体:超越脂质摄取。
Arterioscler Thromb Vasc Biol. 2006 Aug;26(8):1702-11. doi: 10.1161/01.ATV.0000229218.97976.43. Epub 2006 May 25.
9
Phosphatidylserine recognition by phagocytes: a view to a kill.吞噬细胞对磷脂酰丝氨酸的识别:着眼于杀伤作用。
Trends Cell Biol. 2006 Apr;16(4):189-97. doi: 10.1016/j.tcb.2006.02.003. Epub 2006 Mar 10.
10
Trophoblast fusion: fusogenic proteins, syncytins and ADAMs, and other prerequisites for syncytial fusion.滋养层融合:融合蛋白、内源性逆转录病毒包膜糖蛋白和去整合素金属蛋白酶,以及合胞体融合的其他先决条件。
Micron. 2006;37(6):509-17. doi: 10.1016/j.micron.2005.12.011. Epub 2006 Feb 7.

清道夫受体CD36在细胞因子诱导的巨噬细胞融合中发挥作用。

The scavenger receptor CD36 plays a role in cytokine-induced macrophage fusion.

作者信息

Helming Laura, Winter Julia, Gordon Siamon

机构信息

Sir William Dunn School of Pathology, University of Oxford, South Parks Road, Oxford OX1 3RE, UK.

出版信息

J Cell Sci. 2009 Feb 15;122(Pt 4):453-9. doi: 10.1242/jcs.037200. Epub 2009 Jan 20.

DOI:10.1242/jcs.037200
PMID:19155290
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC2714432/
Abstract

Multinucleated giant cells, characteristic of granulomatous infections, originate from the fusion of macrophages. Using an antibody screening strategy we found that the scavenger receptor CD36 participates in macrophage fusion induced by the cytokines IL-4 and GM-CSF. Our results demonstrate that exposure of phosphatidylserine on the cell surface and lipid recognition by CD36 are required for cytokine-induced fusion of macrophages. We also show that CD36 acts in a heterotypic manner during giant-cell formation and that the formation of osteoclasts is independent of CD36. The discovery of molecules involved in the formation of multinucleated giant cells will enable us to determine their functional significance. Furthermore, our results suggest that lipid capture by cell surface receptors may be a general feature of cell fusion.

摘要

多核巨细胞是肉芽肿性感染的特征,由巨噬细胞融合产生。通过抗体筛选策略,我们发现清道夫受体CD36参与细胞因子IL-4和GM-CSF诱导的巨噬细胞融合。我们的结果表明,细胞因子诱导的巨噬细胞融合需要细胞表面磷脂酰丝氨酸的暴露以及CD36对脂质的识别。我们还表明,CD36在巨细胞形成过程中以异型方式发挥作用,并且破骨细胞的形成独立于CD36。参与多核巨细胞形成的分子的发现将使我们能够确定它们的功能意义。此外,我们的结果表明,细胞表面受体对脂质的捕获可能是细胞融合的一个普遍特征。