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000301495 1001_ $$0P:(DE-He78)3877ae274d0271d6bf311bb46539f013$$aDelecluse, Susanne$$b0$$eFirst author$$udkfz
000301495 245__ $$aEpstein-Barr virus induces aberrant B cell migration and diapedesis via FAK-dependent chemotaxis pathways.
000301495 260__ $$a[London]$$bSpringer Nature$$c2025
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000301495 520__ $$aInfection with the Epstein-Barr virus (EBV) is a major risk factor for the development of cancer and autoimmune disorders. The virus enters the body in the pharynx, but EBV causes disease in distant organs, including the gut and the brain. Here we show, using in vitro culture and mouse infection models, that EBV-infected B cells display features of homing cells. Infected B cells undergo migration following paracrine CCL4 release and CCR1 induction, while CCR1 deficiency inhibits migration and, unexpectedly, proliferation of infected B cells. Furthermore, migrating EBV-infected B cells undergo CCL4-dependent diapedesis, induce ICAM-1 on endothelial cells, and disrupt the integrity of endothelial barriers. Both migration and diapedesis are regulated by FAK, with FAK inhibition blocking growth and survival of EBV-transformed B cells, as well as their spreading to spleen and brain in an animal model in vivo. Moreover, IL-10 secreted by EBV-infected B cells attracts and facilitates diapedesis of EBV-negative CD52highCD11c+ B cells, which have reported autoimmune properties. Our results thus provide mechanistic insight on EBV-induced B cell dysregulation, and also hint curbing migration as a potential target for reducing the pathogenicity of EBV-infected B cells.
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000301495 650_7 $$0130068-27-8$$2NLM Chemicals$$aInterleukin-10
000301495 650_7 $$2NLM Chemicals$$aReceptors, CCR1
000301495 650_7 $$0126547-89-5$$2NLM Chemicals$$aIntercellular Adhesion Molecule-1
000301495 650_7 $$0EC 2.7.10.2$$2NLM Chemicals$$aFocal Adhesion Kinase 1
000301495 650_7 $$0EC 2.7.10.2$$2NLM Chemicals$$aPtk2 protein, mouse
000301495 650_2 $$2MeSH$$aAnimals
000301495 650_2 $$2MeSH$$aB-Lymphocytes: virology
000301495 650_2 $$2MeSH$$aB-Lymphocytes: immunology
000301495 650_2 $$2MeSH$$aB-Lymphocytes: metabolism
000301495 650_2 $$2MeSH$$aHerpesvirus 4, Human: physiology
000301495 650_2 $$2MeSH$$aHerpesvirus 4, Human: immunology
000301495 650_2 $$2MeSH$$aMice
000301495 650_2 $$2MeSH$$aHumans
000301495 650_2 $$2MeSH$$aChemotaxis
000301495 650_2 $$2MeSH$$aEpstein-Barr Virus Infections: immunology
000301495 650_2 $$2MeSH$$aEpstein-Barr Virus Infections: virology
000301495 650_2 $$2MeSH$$aEpstein-Barr Virus Infections: pathology
000301495 650_2 $$2MeSH$$aEpstein-Barr Virus Infections: metabolism
000301495 650_2 $$2MeSH$$aInterleukin-10: metabolism
000301495 650_2 $$2MeSH$$aCell Movement
000301495 650_2 $$2MeSH$$aMice, Inbred C57BL
000301495 650_2 $$2MeSH$$aReceptors, CCR1: metabolism
000301495 650_2 $$2MeSH$$aReceptors, CCR1: genetics
000301495 650_2 $$2MeSH$$aIntercellular Adhesion Molecule-1: metabolism
000301495 650_2 $$2MeSH$$aFocal Adhesion Kinase 1: metabolism
000301495 650_2 $$2MeSH$$aEndothelial Cells: metabolism
000301495 650_2 $$2MeSH$$aMice, Knockout
000301495 7001_ $$0P:(DE-He78)0179ab69c93d0c5110458003dbc8af0c$$aBaccianti, Francesco$$b1$$udkfz
000301495 7001_ $$aZala, Manon$$b2
000301495 7001_ $$0P:(DE-He78)704f69971aa28ce8ceb62c6118120ee2$$aSteffens, Alina$$b3
000301495 7001_ $$0P:(DE-He78)07729a8a27f6637e3d284a1441a2cfb7$$aDrenda, Carolin$$b4
000301495 7001_ $$0P:(DE-He78)500ea2412dae05bdfe615df3d9bc2470$$aJudt, Daniel$$b5
000301495 7001_ $$0P:(DE-He78)457c042884c901eb0a02c18bb1d30103$$aHolland-Letz, Tim$$b6$$udkfz
000301495 7001_ $$0P:(DE-He78)27152949302e3bd0d681a6f0548912b9$$aPoirey, Remy$$b7$$udkfz
000301495 7001_ $$00000-0003-1724-4792$$aSujobert, Pierre$$b8
000301495 7001_ $$0P:(DE-He78)25d3c74b949988c637571e696fc04b25$$aDelecluse, Henri-Jacques$$b9$$eLast author$$udkfz
000301495 773__ $$0PERI:(DE-600)2553671-0$$a10.1038/s41467-025-59813-z$$gVol. 16, no. 1, p. 4581$$n1$$p4581$$tNature Communications$$v16$$x2041-1723$$y2025
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