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Membrane vesicles released by intestinal epithelial cells infected with rotavirus inhibit T-cell function

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dc.creatorBarreto, Alfonsospa
dc.creatorRodríguez, Luz-Stellaspa
dc.creatorRojas, Olga Lucíaspa
dc.creatorWolf, Mariespa
dc.creatorGreenberg, Harry B.spa
dc.creatorFranco, Manuel A.spa
dc.creatorAngel, Juanaspa
dc.date.accessioned2020-05-26T00:02:20Z
dc.date.available2020-05-26T00:02:20Z
dc.date.created2010spa
dc.description.abstractRotavirus (RV) predominantly replicates in intestinal epithelial cells (IEC), and 'danger signals' released by these cells may modulate viral immunity. We have recently shown that human model IEC (Caco-2 cells) infected with rhesus-RV release a non-inflammatory group of immunomodulators that includes heat shock proteins (HSPs) and TGF-?1. Here we show that both proteins are released in part in association with membrane vesicles (MV) obtained from filtrated Caco-2 supernatants concentrated by ultracentrifugation. These MV express markers of exosomes (CD63 and others), but not of the endoplasmic reticulum (ER) or nuclei. Larger quantities of proteins associated with MV were released by RV-infected cells than by non-infected cells. VP6 co-immunoprecipitated with CD63 present in these MV, and VP6 co-localized with CD63 in RV-infected cells, suggesting that this viral protein is associated with the MV, and that this association occurs intracellularly. CD63 present in MV preparations from stool samples from 36 children with gastroenteritis due or not due to RV were analyzed. VP6 co-immunoprecipitated with CD63 in 3/8 stool samples from RV-infected children, suggesting that these MV are released by RV-infected cells in vivo. Moreover, fractions that contained MV from RV-infected cells induced death and inhibited proliferation of CD4+ T cells to a greater extent than fractions from non-infected cells. These effects were in part due to TGF-?, because they were reversed by treatment of the T cells with the TGF-?-receptor inhibitor ALK5i. MV from RV-infected and non-infected cells were heterogeneous, with morphologies and typical flotation densities described for exosomes (between 1.10 and 1.18g/mL), and denser vesicles ( and gt;1.24g/mL). Both types of MV from RV-infected cells were more efficient at inhibiting T-cell function than were those from non-infected cells. We propose that RV infection of IEC releases MV that modulate viral immunity. © 2010, Mary Ann Liebert, Inc.eng
dc.format.mimetypeapplication/pdf
dc.identifier.doihttps://doi.org/10.1089/vim.2009.0113
dc.identifier.issn8828245
dc.identifier.urihttps://repository.urosario.edu.co/handle/10336/23474
dc.language.isoengspa
dc.relation.citationEndPage608
dc.relation.citationIssueNo. 6
dc.relation.citationStartPage595
dc.relation.citationTitleViral Immunology
dc.relation.citationVolumeVol. 23
dc.relation.ispartofViral Immunology, ISSN:8828245, Vol.23, No.6 (2010); pp. 595-608spa
dc.relation.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-78650136547&doi=10.1089%2fvim.2009.0113&partnerID=40&md5=347cfaa854dc7b84dc3133227e2389c6spa
dc.rights.accesRightsinfo:eu-repo/semantics/openAccess
dc.rights.accesoAbierto (Texto Completo)spa
dc.source.instnameinstname:Universidad del Rosariospa
dc.source.reponamereponame:Repositorio Institucional EdocURspa
dc.subject.keywordCD63 antigenspa
dc.subject.keywordElectroneng
dc.subject.keywordTransmissioneng
dc.subject.keywordTransforming growth factor beta receptorspa
dc.subject.keywordArticlespa
dc.subject.keywordCD4+ T lymphocytespa
dc.subject.keywordCell deathspa
dc.subject.keywordCell proliferationspa
dc.subject.keywordCell strain CACO 2spa
dc.subject.keywordChildspa
dc.subject.keywordClinical articlespa
dc.subject.keywordControlled studyspa
dc.subject.keywordEndoplasmic reticulumspa
dc.subject.keywordExosomespa
dc.subject.keywordFeces analysisspa
dc.subject.keywordFemalespa
dc.subject.keywordFlotationspa
dc.subject.keywordGastroenteritisspa
dc.subject.keywordHumanspa
dc.subject.keywordHuman cellspa
dc.subject.keywordImmunoprecipitationspa
dc.subject.keywordIn vivo studyspa
dc.subject.keywordIntestine epitheliumspa
dc.subject.keywordMalespa
dc.subject.keywordMembrane vesiclespa
dc.subject.keywordNonhumanspa
dc.subject.keywordRotavirusspa
dc.subject.keywordRotavirus infectionspa
dc.subject.keywordT lymphocytespa
dc.subject.keywordUltracentrifugationspa
dc.subject.keywordVirus immunityspa
dc.subject.keywordAntigenseng
dc.subject.keywordAntigenseng
dc.subject.keywordBlottingeng
dc.subject.keywordCaco-2 Cellsspa
dc.subject.keywordCapsid Proteinsspa
dc.subject.keywordCD4-Positive T-Lymphocytesspa
dc.subject.keywordChildeng
dc.subject.keywordEpitopesspa
dc.subject.keywordExosomesspa
dc.subject.keywordFemalespa
dc.subject.keywordGastroenteritisspa
dc.subject.keywordHeat-Shock Proteinsspa
dc.subject.keywordHumansspa
dc.subject.keywordImmunityeng
dc.subject.keywordInfantspa
dc.subject.keywordIntestinal Mucosaspa
dc.subject.keywordMalespa
dc.subject.keywordMicroscopyeng
dc.subject.keywordMicroscopyeng
dc.subject.keywordPlatelet Membrane Glycoproteinsspa
dc.subject.keywordRotavirus Infectionsspa
dc.subject.keywordTransforming Growth Factor beta1spa
dc.subject.keywordRotavirusspa
dc.titleMembrane vesicles released by intestinal epithelial cells infected with rotavirus inhibit T-cell functionspa
dc.typearticleeng
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersion
dc.type.spaArtículospa
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