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Mutation of E2F2 in mice causes enhanced T lymphocyte proliferation, leading to the development of autoimmunity.

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dc.contributor.authorMurga, Matilde
dc.contributor.authorFernandez-Capetillo, Oscar
dc.contributor.authorField, S J
dc.contributor.authorMoreno, B
dc.contributor.authorBorlado, L R
dc.contributor.authorFujiwara, Y
dc.contributor.authorBalomenos, D
dc.contributor.authorVicario, A
dc.contributor.authorCarrera, A C
dc.contributor.authorOrkin, S H
dc.contributor.authorGreenberg, M E
dc.contributor.authorZubiaga, A M
dc.contributor.funderUnited States Department of Health and Human Serviceses_ES
dc.date.accessioned2024-02-09T14:24:53Z
dc.date.available2024-02-09T14:24:53Z
dc.date.issued2001-12
dc.description.abstractE2Fs are important regulators of proliferation, differentiation, and apoptosis. Here we characterize the phenotype of mice deficient in E2F2. We show that E2F2 is required for immunologic self-tolerance. E2F2(-/-) mice develop late-onset autoimmune features, characterized by widespread inflammatory infiltrates, glomerular immunocomplex deposition, and anti-nuclear antibodies. E2F2-deficient T lymphocytes exhibit enhanced TCR-stimulated proliferation and a lower activation threshold, leading to the accumulation of a population of autoreactive effector/memory T lymphocytes, which appear to be responsible for causing autoimmunity in E2F2-deficient mice. Finally, we provide support for a model to explain E2F2's unexpected role as a suppressor of T lymphocyte proliferation. Rather than functioning as a transcriptional activator, E2F2 appears to function as a transcriptional repressor of genes required for normal S phase entry, particularly E2F1.es_ES
dc.description.peerreviewedSíes_ES
dc.format.number6es_ES
dc.format.page959es_ES
dc.format.volume15es_ES
dc.identifier.citationImmunity . 2001 ;15(6):959-70.es_ES
dc.identifier.doi10.1016/s1074-7613(01)00254-0es_ES
dc.identifier.issn1074-7613es_ES
dc.identifier.journalImmunityes_ES
dc.identifier.pubmedID11754817es_ES
dc.identifier.urihttp://hdl.handle.net/20.500.12105/17701
dc.language.isoenges_ES
dc.publisherCell Presses_ES
dc.relation.publisherversionhttps://doi.org/10.1016/s1074-7613(01)00254-0.es_ES
dc.repisalud.institucionCNIOes_ES
dc.repisalud.orgCNIOCNIO::Grupos de investigación::Grupo de Inestabilidad Genómicaes_ES
dc.rights.accessRightsopen accesses_ES
dc.rights.licenseAttribution-NonCommercial-NoDerivatives 4.0 Internacional*
dc.rights.urihttp://creativecommons.org/licenses/by-nc-nd/4.0/*
dc.subject.meshCell Cycle Proteinses_ES
dc.subject.meshDNA-Binding Proteinses_ES
dc.subject.meshAnimalses_ES
dc.subject.meshApoptosises_ES
dc.subject.meshAutoimmune Diseaseses_ES
dc.subject.meshAutoimmunityes_ES
dc.subject.meshCell Divisiones_ES
dc.subject.meshChimeraes_ES
dc.subject.meshClonal Deletiones_ES
dc.subject.meshE2F Transcription Factorses_ES
dc.subject.meshE2F1 Transcription Factores_ES
dc.subject.meshE2F2 Transcription Factores_ES
dc.subject.meshGene Expression Regulationes_ES
dc.subject.meshGlomerulonephritis, Membranoproliferativees_ES
dc.subject.meshH-Y Antigenes_ES
dc.subject.meshHumanses_ES
dc.subject.meshImmunologic Memoryes_ES
dc.subject.meshInflammationes_ES
dc.subject.meshJurkat Cellses_ES
dc.subject.meshLymphocyte Activationes_ES
dc.subject.meshMalees_ES
dc.subject.meshMicees_ES
dc.subject.meshMice, Inbred BALB Ces_ES
dc.subject.meshMice, Inbred C57BLes_ES
dc.subject.meshMice, Knockoutes_ES
dc.subject.meshMutagenesis, Site-Directedes_ES
dc.subject.meshReceptors, Antigen, T-Celles_ES
dc.subject.meshRecombinant Fusion Proteinses_ES
dc.subject.meshRepressor Proteinses_ES
dc.subject.meshS Phasees_ES
dc.subject.meshSelf Tolerancees_ES
dc.subject.meshSplenomegalyes_ES
dc.subject.meshT-Lymphocyteses_ES
dc.subject.meshThymus Glandes_ES
dc.subject.meshTranscription Factorses_ES
dc.subject.meshTransfectiones_ES
dc.titleMutation of E2F2 in mice causes enhanced T lymphocyte proliferation, leading to the development of autoimmunity.es_ES
dc.typejournal articlees_ES
dc.type.hasVersionVoRes_ES
dspace.entity.typePublication
relation.isAuthorOfPublication109ab297-8df3-458e-9a03-0dd210ea8e09
relation.isAuthorOfPublicationeb478d8c-dd11-4b47-8795-7ac57cb60b2d
relation.isAuthorOfPublication.latestForDiscovery109ab297-8df3-458e-9a03-0dd210ea8e09
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