T-cell antagonism by short half-life pMHC ligands can be mediated by an efficient trapping of T-cell polarization toward the APC

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dc.contributor.authorCarreno, Leandro J.
dc.contributor.authorRiquelme, Erick M.
dc.contributor.authorGonzalez, Pablo A.
dc.contributor.authorEspagnolle, Nicolas
dc.contributor.authorRiedel, Claudia A.
dc.contributor.authorValitutti, Salvatore
dc.contributor.authorKalergis, Alexis M.
dc.date.accessioned2024-01-10T12:09:10Z
dc.date.available2024-01-10T12:09:10Z
dc.date.issued2010
dc.description.abstractT-cell activation results from productive T-cell receptor (TCR) engagement by a cognate peptide-MHC (pMHC) complex on the antigen presenting cell (APC) surface, a process leading to the polarization of the T-cell secretory machinery toward the APC interface. We have previously shown that the half-life of the TCR/pMHC interaction and the density of pMHC on the APC are two parameters determining T-cell activation. However, whether the half-life of the TCR/pMHC interaction can modulate the efficiency of T-cell secretory machinery polarization toward an APC still remains unclear. Here, by using altered peptide ligands conferring different half-lives to the TCR/pMHC interaction, we have tested how this parameter can control T-cell polarization. We observed that only TCR/pMHC interactions with intermediate half-lives can promote the assembly of synapses that lead to T-cell activation. Strikingly, intermediate half-life interactions can be competed out by short half-life interactions, which can efficiently promote T-cell polarization and antagonize T-cell activation that was induced by activating intermediate half-life interactions. However, short TCR/pMHC interactions fail at promoting phosphorylation of signaling molecules at the T-cell-APC contact interface, which are needed for T-cell activation. Our data suggest that although intermediate half-life pMHC ligands promote assembly of activating synapses, this process can be inhibited by short half-life antagonistic pMHC ligands, which promote the assembly of non activating synapses.
dc.description.funderFondo Nacional de Desarrollo Cientifico Tecnologico (FONDECYT)
dc.description.funderFondo de Fomento al Desarrollo Cientifico y Tecnologico (FONDEF)
dc.description.funderComision Nacional de Investigacion Cientifica y Tecnologica CONICYT
dc.fechaingreso.objetodigital2024-05-06
dc.format.extent6 páginas
dc.fuente.origenWOS
dc.identifier.doi10.1073/pnas.0911258107
dc.identifier.issn0027-8424
dc.identifier.pubmedidMEDLINE:20075022
dc.identifier.urihttps://doi.org/10.1073/pnas.0911258107
dc.identifier.urihttps://repositorio.uc.cl/handle/11534/76465
dc.identifier.wosidWOS:000273559200037
dc.information.autorucCiencias Biológicas;Carreño L;S/I;120819
dc.information.autorucCiencias Biológicas;González PA;S/I;15616
dc.information.autorucCiencias Biológicas;Kalergis A;S/I;90610
dc.information.autorucCiencias Biológicas;Riedel CA;S/I;88772
dc.information.autorucCiencias Biológicas;Riquelme EM;S/I;1001194
dc.issue.numero1
dc.language.isoen
dc.nota.accesocontenido parcial
dc.pagina.final215
dc.pagina.inicio210
dc.publisherNATL ACAD SCIENCES
dc.revistaPROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA
dc.rightsacceso restringido
dc.subjectimmunological synapse
dc.subjectT-cell receptor
dc.subjectT-cell receptor half-life
dc.subjectdendritic cells
dc.subjectANTIGEN-PRESENTING CELL
dc.subjectPEPTIDE-MHC COMPLEXES
dc.subjectIMMUNOLOGICAL SYNAPSE
dc.subjectRECEPTOR BINDING
dc.subjectTCR ENGAGEMENT
dc.subjectDWELL-TIME
dc.subjectACTIVATION
dc.subjectRECOGNITION
dc.subjectMODULATION
dc.subjectSELECTION
dc.subject.ods03 Good Health and Well-being
dc.subject.odspa03 Salud y bienestar
dc.titleT-cell antagonism by short half-life pMHC ligands can be mediated by an efficient trapping of T-cell polarization toward the APC
dc.typeartículo
dc.volumen107
sipa.codpersvinculados120819
sipa.codpersvinculados15616
sipa.codpersvinculados90610
sipa.codpersvinculados88772
sipa.codpersvinculados1001194
sipa.indexWOS
sipa.indexScopus
sipa.trazabilidadCarga SIPA;09-01-2024
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