Murga, MatildeFernandez-Capetillo, OscarField, S JMoreno, BBorlado, L RFujiwara, YBalomenos, DVicario, ACarrera, A COrkin, S HGreenberg, M EZubiaga, A M2024-02-092024-02-092001-12Immunity . 2001 ;15(6):959-70.1074-7613http://hdl.handle.net/20.500.12105/17701E2Fs 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.engVoRhttp://creativecommons.org/licenses/by-nc-nd/4.0/Cell Cycle ProteinsDNA-Binding ProteinsAnimalsApoptosisAutoimmune DiseasesAutoimmunityCell DivisionChimeraClonal DeletionE2F Transcription FactorsE2F1 Transcription FactorE2F2 Transcription FactorGene Expression RegulationGlomerulonephritis, MembranoproliferativeH-Y AntigenHumansImmunologic MemoryInflammationJurkat CellsLymphocyte ActivationMaleMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMutagenesis, Site-DirectedReceptors, Antigen, T-CellRecombinant Fusion ProteinsRepressor ProteinsS PhaseSelf ToleranceSplenomegalyT-LymphocytesThymus GlandTranscription FactorsTransfectionAttribution-NonCommercial-NoDerivatives 4.0 Internacional1175481715695910.1016/s1074-7613(01)00254-0Immunityopen access