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dc.creatorMonel, Blandine 
dc.creatorMcKeon, Annmarie 
dc.creatorLamothe-Molina, Pedro 
dc.creatorJani, Priya 
dc.creatorBoucau, Julie 
dc.creatorPacheco Nieva, Yovana 
dc.creatorJones, R. Brad 
dc.creatorLe Gall, Sylvie 
dc.creatorWalker, Bruce D. 
dc.date.accessioned2020-05-26T00:03:57Z
dc.date.available2020-05-26T00:03:57Z
dc.date.created2019
dc.identifier.issn22111247
dc.identifier.urihttps://repository.urosario.edu.co/handle/10336/23642
dc.description.abstract"Even with sustained antiretroviral therapy, resting CD4 + T cells remain a persistent reservoir of HIV infection, representing a critical barrier to curing HIV. Here, we demonstrate that CD8 + T cells recognize infected, non-activated CD4 + T cells in the absence of de novo protein production, as measured by immune synapse formation, degranulation, cytokine production, and killing of infected cells. Immune recognition is induced by HLA-I presentation of peptides derived from incoming viral particles, and recognition occurred either following cell-free virus infection or following cell-to-cell spread. CD8 + T cells from HIV controllers mediate more effective immune recognition than CD8 + T cells from progressors. These results indicate that non-activated HIV-infected CD4 + T cells can be targeted by CD8 + T cells directly after HIV entry, before reverse transcription, and thus before the establishment of latency, and suggest a mechanism whereby the immune response may reduce the size of the HIV reservoir. The cure for HIV is not achievable due to HIV reservoirs, mostly in resting CD4 + T cells. Monel et al. show that CD8 + T cells from HIV controllers are able to establish immunological synapses with HIV + resting CD4 + T cells, leading to IFN-?, MIP1-? production, degranulation, and the elimination of the target cells. © 2019 The Authors"
dc.format.mimetypeapplication/pdf
dc.language.isoeng
dc.relation.ispartofCell Reports, ISSN:22111247, Vol.27, No.1 (2019); pp. 142-153.e4
dc.relation.urihttps://www.scopus.com/inward/record.uri?eid=2-s2.0-85063383455&doi=10.1016%2fj.celrep.2019.03.016&partnerID=40&md5=332d50ba72513d6eed03a3e1bef75e1c
dc.sourceinstname:Universidad del Rosario
dc.sourcereponame:Repositorio Institucional EdocUR
dc.titleHIV Controllers Exhibit Effective CD8 + T Cell Recognition of HIV-1-Infected Non-activated CD4 + T Cells
dc.typearticle
dc.publisherElsevier B.V.
dc.subject.keywordT lymphocyte receptor
dc.subject.keywordAntigen presentation
dc.subject.keywordArticle
dc.subject.keywordCD4+ T lymphocyte
dc.subject.keywordCD8+ T lymphocyte
dc.subject.keywordColorimetry
dc.subject.keywordControlled study
dc.subject.keywordCytokine production
dc.subject.keywordDegranulation
dc.subject.keywordFlow cytometry
dc.subject.keywordFluorescence microscopy
dc.subject.keywordFluorescence resonance energy transfer
dc.subject.keywordHuman
dc.subject.keywordHuman cell
dc.subject.keywordHuman immunodeficiency virus 1 infection
dc.subject.keywordImmune response
dc.subject.keywordImmunological synapse
dc.subject.keywordLong terminal repeat
dc.subject.keywordMolecular recognition
dc.subject.keywordPriority journal
dc.subject.keywordProtein cleavage
dc.subject.keywordProtein protein interaction
dc.subject.keywordSynapse
dc.subject.keywordVirus entry
dc.subject.keywordVirus genome
dc.subject.keywordVirus particle
dc.subject.keywordCytotoxic T lymphocytes
dc.subject.keywordElite controllers
dc.subject.keywordGranzyme
dc.subject.keywordHIV
dc.subject.keywordHIV cure
dc.subject.keywordHLA
dc.subject.keywordImmunologic synapse
dc.subject.keywordPerforin
dc.rights.accesRightsinfo:eu-repo/semantics/openAccess
dc.type.spaArtículo
dc.rights.accesoAbierto (Texto Completo)
dc.type.hasVersioninfo:eu-repo/semantics/publishedVersion
dc.identifier.doihttps://doi.org/10.1016/j.celrep.2019.03.016
dc.relation.citationEndPage153.e4
dc.relation.citationIssueNo. 1
dc.relation.citationStartPage142
dc.relation.citationTitleCell Reports
dc.relation.citationVolumeVol. 27


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