2024
Increasing the Level of Knock-in of a Construct Encoding the HIV-1 Fusion Inhibitor, MT-C34 Peptide, into the <i>CXCR4</i> Locus in the CEM/R5 T Cell Line
Golubev D, Komkov D, Shepelev M, Mazurov D, Kruglova N. Increasing the Level of Knock-in of a Construct Encoding the HIV-1 Fusion Inhibitor, MT-C34 Peptide, into the CXCR4 Locus in the CEM/R5 T Cell Line. Молекулярная Биология 2024, 58 DOI: 10.31857/s0026898424040044.Peer-Reviewed Original ResearchNuclear localization signalNonhomologous end-joining pathwayEnd-joining pathwayKnock-inKnock-in modelDNA repairDNA-dependent protein kinase inhibitorT cell linesBlock DNA repairGenome editing technologyPeptide fusion inhibitorsTranscription factor NF-kBLocalization signalCXCR4 locusDonor plasmidCas9 nucleaseCas9 proteinDNA modificationsPrimary human cellsProtein kinase inhibitorsHIV-1Transporter sequencesInhibit DNA repairPlasmid transportEffective gene therapy approachMethods to Increase the Efficiency of Knock-in of a Construct Encoding the HIV-1 Fusion Inhibitor, MT-C34 Peptide, into the CXCR4 Locus in the CEM/R5 T Cell Line
Golubev D, Komkov D, Shepelev M, Mazurov D, Kruglova N. Methods to Increase the Efficiency of Knock-in of a Construct Encoding the HIV-1 Fusion Inhibitor, MT-C34 Peptide, into the CXCR4 Locus in the CEM/R5 T Cell Line. Molecular Biology 2024, 58: 658-671. DOI: 10.1134/s0026893324700249.Peer-Reviewed Original ResearchNuclear localization signalNonhomologous End JoiningDNA nuclear targeting sequencesKnock-inCXCR4 locusDNA repairT cell linesNonhomologous end-joining pathwayNuclear targeting sequenceDNA-dependent protein kinase inhibitorBlock DNA repairHIV-1Knock-in efficiencyEffective gene therapy approachGenome editing technologyTranscription factor NF-kBLocalization signalTreat HIV infectionGene therapy approachesTarget sequenceDonor plasmidCas9 nucleaseCas9 proteinEnd joiningDNA modificationsEfficient editing of the CXCR4 locus using Cas9 ribonucleoprotein complexes stabilized with polyglutamic acid
Golubev D, Komkov D, Shepelev M, Mazurov D, Kruglova N. Efficient editing of the CXCR4 locus using Cas9 ribonucleoprotein complexes stabilized with polyglutamic acid. Доклады Российской Академии Наук Науки О Жизни 2024, 514: 85-90. DOI: 10.31857/s2686738924010164.Peer-Reviewed Original Research[Donor DNA Modification with Cas9 Targeting Sites Improves the Efficiency of MTC34 Knock-in into the CXCR4 Locus].
Shepelev M, Komkov D, Golubev D, Borovikova S, Mazurov D, Kruglova N. [Donor DNA Modification with Cas9 Targeting Sites Improves the Efficiency of MTC34 Knock-in into the CXCR4 Locus]. Молекулярная Биология 2024, 58: 590-600. PMID: 39709563, DOI: 10.31857/s0026898424040058, edn: incoyt.Peer-Reviewed Original ResearchConceptsCas9 target sitesDouble-strand breaksCell genomeGenetic constructsDonor DNAKnock-inDonor plasmid DNAKnock-in efficiencyGenome editing technologyInduce double-strand breaksProximal nucleotidesPAM sitesDonor plasmidDonor sequenceDNA modificationsGenomeIn vitroInduced cleavageCRISPR/Cas9 systemCas9Editing technologyDNAPlasmid DNAT cell linesTarget cell genome
2023
Efficient Editing of the CXCR4 Locus Using Cas9 Ribonucleoprotein Complexes Stabilized with Polyglutamic Acid
Golubev D, Komkov D, Shepelev M, Mazurov D, Kruglova N. Efficient Editing of the CXCR4 Locus Using Cas9 Ribonucleoprotein Complexes Stabilized with Polyglutamic Acid. Doklady Biological Sciences 2023, 513: s28-s32. PMID: 38190037, DOI: 10.1134/s0012496623700862.Peer-Reviewed Original ResearchSeparation of B- and T-Cell-Specific Signaling Molecules Prevents Oncogenic Transformation in Lymphoid Malignancies
Ketzer F, Klemm L, Robinson M, Loucks C, Arce D, Cosgun K, Kothari S, Müschen M. Separation of B- and T-Cell-Specific Signaling Molecules Prevents Oncogenic Transformation in Lymphoid Malignancies. Blood 2023, 142: 1396. DOI: 10.1182/blood-2023-189221.Peer-Reviewed Original ResearchKinase ZAP70Transcriptional regulationTranscription factorsKinase SykDownstream activationT-cell signaling proteinsCRISPR/Cas9-mediated knockoutComparative proteomic analysisNegative selectionFunction of proteinsWild-type cellsCas9-mediated knockoutCo-expressed proteinsPre-malignant cellsT cell linesCellular fitnessTranscription machinerySLP-76Signaling proteinsMalignant transformationSignal transductionAberrant transcriptionProteomic analysisChIP-qPCRNovel key mechanism
2022
Concurrent IRF4 Rearrangements in a Patient with B Cell and T Cell Disorders
Bernhisel A, Siddon A, Katz S. Concurrent IRF4 Rearrangements in a Patient with B Cell and T Cell Disorders. American Journal Of Clinical Pathology 2022, 158: s105-s105. DOI: 10.1093/ajcp/aqac126.221.Peer-Reviewed Original ResearchDiffuse large B-cell lymphomaIRF4 rearrangementB cellsCD30-positive T-cell lymphoproliferative disordersT-cell lymphoproliferative disorderLarge B-cell lymphomaPast medical historyT-cell lesionsCell lymphoproliferative disordersT-cell disordersB-cell lymphomaT-cell neoplasmsT cell linesIRF4 gene rearrangementT cell developmentLymphomatoid papulosisHodgkin's diseaseHematopoietic progenitor cellsLymphoproliferative disordersIntroduction/ObjectiveCase reportMedical historyCommon lymphoid progenitorsCell lesionsCell neoplasmsEngineering T-Cell Resistance to HIV-1 Infection via Knock-In of Peptides from the Heptad Repeat 2 Domain of gp41
Maslennikova A, Kruglova N, Kalinichenko S, Komkov D, Shepelev M, Golubev D, Siniavin A, Vzorov A, Filatov A, Mazurov D. Engineering T-Cell Resistance to HIV-1 Infection via Knock-In of Peptides from the Heptad Repeat 2 Domain of gp41. MBio 2022, 13: e03589-21. PMID: 35073736, PMCID: PMC8787484, DOI: 10.1128/mbio.03589-21.Peer-Reviewed Original ResearchConceptsHIV-1 infectionCD4 lymphocytesHIV-1Antiretroviral therapyLentiviral vectorsT cellsHeptad repeat 2Resistance to HIV-1 infectionTherapy of HIV infectionInhibitors of HIV-1 entryHIV-1 proviral DNATherapeutic lentiviral vectorInhibitors of HIV-1 fusionHIV-1 entryKnock-inCell surfaceT cell linesHIV-1 fusionProtection of lymphocytesKnock-in (KIGene modificationLatent provirusesHIV infectionViral clearanceFusion inhibitory peptides
2020
Use of CART cells to selectively target autoantigen-specific T cells for the treatment of autoimmune diabetes
Yu H, Bettini M, Ellis G, Riley J, Collins J, Preston-Hurlburt P, Korah M, Mallone R, Deng S, Wang X, Fremont D, Spiegel D, Cresswell P, Herold K. Use of CART cells to selectively target autoantigen-specific T cells for the treatment of autoimmune diabetes. The Journal Of Immunology 2020, 204: 238.8-238.8. DOI: 10.4049/jimmunol.204.supp.238.8.Peer-Reviewed Original ResearchCART cellsT cellsAutoimmune diabetesCAR constructsHuman antigen-specific CD8Autoantigen-specific T cellsAntigen-specific CD8Pathogenic T cellsPrevious clinical trialsΒ-cell damageChimeric antigen receptorNon-specific actionT cell linesHuman T cellsDominant cell typeHuman insulitisPathogenic subpopulationsNovel immunotherapiesPrimary human T cellsClinical trialsPrimary mediatorPeptide epitopesAntigen receptorMicroglobulin complexCAR signalingHSV-2 infects T follicular helper cells to promote HIV reactivation
Pierce C, Loh L, Preston-Hurlburt P, Herold K, Herold B. HSV-2 infects T follicular helper cells to promote HIV reactivation. The Journal Of Immunology 2020, 204: 247.24-247.24. DOI: 10.4049/jimmunol.204.supp.247.24.Peer-Reviewed Original ResearchCD4 T cellsFollicular helper cellsHIV reactivationHSV-2T cellsTfh cellsIL-32Helper cellsSystemic effectsCD4 T-cell subpopulationsT Follicular Helper CellsHSV-2 recurrencesHSV-2 seropositiveT cell subpopulationsGlobal HIV epidemicPotential systemic effectsT cell linesSeronegative womenIL-32γHigh HIVViral loadHIV transmissionLatent HIVProinflammatory cytokinesHIV epidemicDevelopment of a Brigatinib degrader (SIAIS117) as a potential treatment for ALK positive cancer resistance
Sun N, Ren C, Kong Y, Zhong H, Chen J, Li Y, Zhang J, Zhou Y, Qiu X, Lin H, Song X, Yang X, Jiang B. Development of a Brigatinib degrader (SIAIS117) as a potential treatment for ALK positive cancer resistance. European Journal Of Medicinal Chemistry 2020, 193: 112190. PMID: 32179332, DOI: 10.1016/j.ejmech.2020.112190.Peer-Reviewed Original ResearchMeSH KeywordsAnaplastic Lymphoma KinaseAntineoplastic AgentsCarcinoma, Non-Small-Cell LungCell Line, TumorCell ProliferationDose-Response Relationship, DrugDrug DevelopmentDrug Resistance, NeoplasmDrug Screening Assays, AntitumorHEK293 CellsHumansLung NeoplasmsMolecular Docking SimulationMolecular StructureProtein Kinase InhibitorsStructure-Activity RelationshipConceptsAnaplastic large cell lymphomaCell lung cancerLung cancerALK proteinNon-small cell lung cancerDrug resistanceSmall cell lung cancerLarge cell lymphomaPotential therapeutic strategyAnti-proliferation abilityCell linesNPM-ALK fusion proteinT cell linesCancer cell linesEML4-ALKCancer regressionTherapeutic strategiesPotential treatmentGrowth inhibition effectInhibitor drugsALK activityCancerCancer resistanceBrigatinibLymphoma
2019
Tyrosine kinase inhibition to improve anthracycline-based chemotherapy efficacy in T-cell lymphoma
Magni M, Biancon G, Rizzitano S, Cavanè A, Paolizzi C, Dugo M, Corradini P, Carniti C. Tyrosine kinase inhibition to improve anthracycline-based chemotherapy efficacy in T-cell lymphoma. British Journal Of Cancer 2019, 121: 567-577. PMID: 31474759, PMCID: PMC6889385, DOI: 10.1038/s41416-019-0557-8.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntineoplastic Combined Chemotherapy ProtocolsApoptosisCell CycleCell SurvivalCyclophosphamideDasatinibDoxorubicinDrug Administration ScheduleDrug SynergismEtoposideGene ExpressionGene Expression ProfilingHumansJurkat CellsLymphoma, T-CellMice, Inbred NODMice, SCIDPrednisoneProtein Kinase InhibitorsProtein-Tyrosine KinasesProto-Oncogene Proteins c-fynReceptors, Antigen, T-CellrhoA GTP-Binding ProteinTreatment OutcomeUp-RegulationVincristineConceptsT-cell lymphomaPeripheral T-cell lymphomaDrug combinationsTyrosine kinase inhibitor dasatinibVivo xenograft mouse modelMalignant T-cell linesXenograft mouse modelTyrosine kinase inhibitionTumor growth inhibitionKinase inhibitor dasatinibT cell receptorT cell linesT-cell receptor pathwayCell cycle distributionWestern blot analysisChemotherapy efficacyPreclinical modelsConclusionsOur dataMouse modelVivo effectsXenograft modelClinical testingTreatment resultsInhibitor dasatinibLymphoma
2014
A Humanized Mouse Model of Autoimmune Insulitis
Milam A, Maher SE, Gibson JA, Lebastchi J, Wen L, Ruddle NH, Herold KC, Bothwell AL. A Humanized Mouse Model of Autoimmune Insulitis. Diabetes 2014, 63: 1712-1724. PMID: 24478396, PMCID: PMC3994947, DOI: 10.2337/db13-1141.Peer-Reviewed Original ResearchConceptsT cellsDiabetic donorsInsulin stainingMouse modelAntigen-pulsed cellsAutoantigen-derived peptidesNOD mouse modelHumanized mouse modelType 1 diabetesPancreatic β-cellsT cell linesHuman T cellsIslet infiltrationAutoimmune diabetesNOD-SCIDAutoimmune insulitisHuman diabetesDestructive infiltrationMouse isletsMechanism of inductionΒ-cellsDiabetesDiabetes researchDisease modelsInsulitis104 Cell-to-cell transmission of HIV
Mazurov D, Filatov A. 104 Cell-to-cell transmission of HIV. JAIDS Journal Of Acquired Immune Deficiency Syndromes 2014, 65: 40. PMCID: PMC4149629, DOI: 10.1097/01.qai.0000446684.24980.4f.Peer-Reviewed Original ResearchCell-to-cell transmission of HIVCell-to-cell transmissionTransmission of HIVVirological synapseTarget cellsHIV cell-to-cell transmissionCD4+ T lymphocytesModel of HIV transmissionSurface of effector cellsCell-to-cell infectionCell-to-cell viral transmissionCell-free infectionResistance of HIVPeripheral lymph nodesModified target cellsFormation of intercellular contactsHIV surface protein gp120Infected cellsT cell linesFree viral particlesEffector cellsIntercellular adhesive junctionsLymph nodesT lymphocytesCD4 receptor
2013
MHC Class I–Associated Phosphopeptides Are the Targets of Memory-like Immunity in Leukemia
Cobbold M, De La Peña H, Norris A, Polefrone JM, Qian J, English AM, Cummings KL, Penny S, Turner JE, Cottine J, Abelin JG, Malaker SA, Zarling AL, Huang HW, Goodyear O, Freeman SD, Shabanowitz J, Pratt G, Craddock C, Williams ME, Hunt DF, Engelhard VH. MHC Class I–Associated Phosphopeptides Are the Targets of Memory-like Immunity in Leukemia. Science Translational Medicine 2013, 5: 203ra125. PMID: 24048523, PMCID: PMC4071620, DOI: 10.1126/scitranslmed.3006061.Peer-Reviewed Original ResearchConceptsT cellsImmune surveillanceAllogeneic stem cell transplantationMajor histocompatibility complex class IStem cell transplantationT cell responsesHistocompatibility complex class IAdoptive transfer immunotherapyCancer immune surveillanceHuman leukocyte antigenComplex class ICell linesPrimary leukemia cellsT cell linesClinical outcomesCell transplantationLeukocyte antigenLeukemia patientsMemory compartmentHematological tumorsHealthy individualsLeukemia cell linesCell responsesMalignant transformationNormal tissues
2010
VEGF Blockade Inhibits Lymphocyte Recruitment and Ameliorates Immune-Mediated Vascular Remodeling
Zhang J, Silva T, Yarovinsky T, Manes TD, Tavakoli S, Nie L, Tellides G, Pober JS, Bender JR, Sadeghi MM. VEGF Blockade Inhibits Lymphocyte Recruitment and Ameliorates Immune-Mediated Vascular Remodeling. Circulation Research 2010, 107: 408-417. PMID: 20538685, PMCID: PMC2929975, DOI: 10.1161/circresaha.109.210963.Peer-Reviewed Original ResearchMeSH KeywordsAngiogenesis InhibitorsAnimalsAntibodies, MonoclonalAntibodies, Monoclonal, HumanizedArteriesBevacizumabCD3 ComplexCoronary VesselsHumansJurkat CellsLymphocytesMiceMice, SCIDReceptors, Vascular Endothelial Growth FactorT-LymphocytesTransplantation, HeterologousVascular Endothelial Growth Factor AConceptsVascular endothelial growth factorRole of VEGFAdhesion molecule-1T cellsVascular remodelingHuman T cellsMolecule-1Recombinant intercellular adhesion molecule-1Human arteriesVascular cell adhesion molecule-1Intercellular adhesion molecule-1Cell adhesion molecule-1Inhibition of VEGFT cell accumulationPeripheral blood mononuclearEffects of VEGFSubpopulation of CD3Novel therapeutic approachesEndothelial growth factorT cell activationT cell linesVEGFR-1 mRNAT cell captureLymphocyte recruitmentBlood mononuclear
2009
Engineered Interleukin-2 Antagonists for the Inhibition of Regulatory T Cells
Liu DV, Maier LM, Hafler DA, Wittrup KD. Engineered Interleukin-2 Antagonists for the Inhibition of Regulatory T Cells. Journal Of Immunotherapy 2009, 32: 887-894. PMID: 19816193, PMCID: PMC4078882, DOI: 10.1097/cji.0b013e3181b528da.Peer-Reviewed Original ResearchConceptsIL-2 receptorRegulatory T cellsWild-type IL-2IL-2T cellsIL-2 analogHigh regulatory T cellsIL-2 receptor alphaRegulatory T-cell suppressionInterleukin-2 antagonistsAntitumor immune responseT cell suppressionIL-2 receptor alpha subunitT cell growthT cell linesTreg inhibitionImmunosuppressive effectsCancer patientsSimilar efficacyImmune responseReceptor alpha subunitCell suppressionReceptor alphaAlpha subunitHuman interleukinRACK-1 overexpression protects against goniothalamin-induced cell death
Inayat-Hussain S, Wong L, Chan K, Rajab N, Din L, Harun R, Kizilors A, Saxena N, Mourtada-Maarabouni M, Farzaneh F, Williams G. RACK-1 overexpression protects against goniothalamin-induced cell death. Toxicology Letters 2009, 191: 118-122. PMID: 19698770, PMCID: PMC2845802, DOI: 10.1016/j.toxlet.2009.08.012.Peer-Reviewed Original ResearchConceptsRACK-1Cell deathProtein C kinase 1C kinase 1Full-length receptorDNA strand breaksDNA damageStable transfectantsStrand breaksTumor cell linesCell linesOverexpressionT cell linesApoptosisClonogenic assayPotential roleCellsCrucial roleGoniothalaminGenesTransfectantsJurkatPathwayCytotoxic agentsCytotoxicity
2008
The human T cell receptor Vβ repertoire of normal peripheral blood lymphocytes before and after mitogen stimulation
WONG F, HIBBERD M, WEN L, MILLWARD B, DEMAINF A. The human T cell receptor Vβ repertoire of normal peripheral blood lymphocytes before and after mitogen stimulation. Clinical & Experimental Immunology 2008, 92: 361-366. PMID: 8387412, PMCID: PMC1554814, DOI: 10.1111/j.1365-2249.1993.tb03405.x.Peer-Reviewed Original ResearchConceptsT cellsMitogen stimulationT cell antigen receptorPolymerase chain reactionT cell receptor Vβ repertoireFlow cytometryNormal peripheral blood lymphocytesMitogen-stimulated T cellsPeripheral blood lymphocytesTCR gene usagePeripheral T cellsT cell linesVβ repertoireUnstimulated T cellsBeta repertoireBlood lymphocytesHealthy individualsPCR methodBeta 6Cell antigen receptorGene usageAntigen receptorBeta 2Beta 5Chain reactionA novel CD4 T-cell epitope described from one of the cervical cancer patients vaccinated with HPV 16 or 18 E7-pulsed dendritic cells
Wang X, Santin AD, Bellone S, Gupta S, Nakagawa M. A novel CD4 T-cell epitope described from one of the cervical cancer patients vaccinated with HPV 16 or 18 E7-pulsed dendritic cells. Cancer Immunology, Immunotherapy 2008, 58: 301-308. PMID: 18446336, PMCID: PMC2782377, DOI: 10.1007/s00262-008-0525-2.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAntigen PresentationCancer VaccinesCD4 AntigensDendritic CellsDose-Response Relationship, DrugEpitopes, T-LymphocyteFemaleHistocompatibility Antigens Class IHistocompatibility Antigens Class IIHuman papillomavirus 16Human papillomavirus 18HumansMolecular Sequence DataNeoplasm StagingOncogene Proteins, ViralPapillomavirus E7 ProteinsSignal TransductionT-LymphocytesUterine Cervical NeoplasmsConceptsT cell epitopesCD4 T cell epitopesT cell responsesT cell clonesHPV 16T cell linesDose escalation phase I clinical trialPeripheral blood mononuclear cellsE7 proteinPositive T-cell responsesPhase I clinical trialAutologous mature DCDendritic cell vaccinationIIA cervical cancerCervical cancer patientsIFN-γ secretionBlood mononuclear cellsHuman papillomavirus type 16Papillomavirus type 16Cell vaccinationStage IBDendritic cellsMature DCsCervical cancerELISPOT assay
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