2025
High affinity CD16 polymorphism associated with reduced risk of severe COVID-19
Qualls A, Tsao T, Lui I, Lim S, Su Y, Chen E, Duchen D, Maecker H, Kim-Schulze S, Montgomery R, Krammer F, Langelier C, Levy O, Baden L, Melamed E, Ehrlich L, McComsey G, Sekaly R, Cairns C, Haddad E, Shaw A, Hafler D, Corry D, Kheradmand F, Atkinson M, Brakenridge S, Higuita N, Metcalf J, Hough C, Messer W, Pulendran B, Nadeau K, Davis M, Fernandez-Sesma A, Simon V, Kraft M, Bime C, Calfee C, Erle D, Schaenmann J, Ozonoff A, Peters B, Kleinstein S, Augustine A, Diray-Arce J, Becker P, Rouphael N, Network I, Goldman J, Calabrese D, Heath J, Wells J, Reed E, Lanier L, Pickering H, Aguilar O. High affinity CD16 polymorphism associated with reduced risk of severe COVID-19. JCI Insight 2025 PMID: 40402577, DOI: 10.1172/jci.insight.191314.Peer-Reviewed Original ResearchAntibody-dependent cellular cytotoxicitySevere COVID-19Anti-SARS-CoV-2 IgG titersNK cell-mediated immune responsesNK cell-mediated antibody-dependent cellular cytotoxicityHost-directed therapeutic strategiesSevere disease trajectoryCell-mediated immune responsesHospitalized COVID-19 patientsLevels of inflammatory mediatorsNatural killer cellsSevere respiratory complicationsImmunopathogenesis of COVID-19Activating Fc receptorsRisk of ICU admissionRisk of severe COVID-19SARS-CoV-2 infectionCOVID-19 patientsCOVID-19 cohortIn vitro reporter systemKiller cellsRespiratory complicationsCellular cytotoxicityViral loadImmunophenotypic assessment
2024
A Phase 1 randomized trial of homologous and heterologous filovirus vaccines with a late booster dose
Rostad C, Yildirim I, Kao C, Yi J, Kamidani S, Peters E, Stephens K, Gibson T, Hsiao H, Singh K, Spearman P, McCracken C, Agbakoba V, Tomashek K, Goll J, Gelber C, Johnson R, Lee S, Maner-Smith K, Bosinger S, Ortlund E, Chen X, Anderson L, Wrammert J, Suthar M, Rouphael N, Anderson E. A Phase 1 randomized trial of homologous and heterologous filovirus vaccines with a late booster dose. Npj Vaccines 2024, 9: 255. PMID: 39715748, PMCID: PMC11666633, DOI: 10.1038/s41541-024-01042-4.Peer-Reviewed Original ResearchAntibody-dependent cellular cytotoxicityMVA-BNPrime-boostHeterologous prime-boost strategyPrime-boost schedulePhase 1 trialSevere viral hemorrhagic feverPrime-boost strategyHealthy U.S. adultsHomologous prime-boostViral hemorrhagic feverGlobal health priorityCellular responsesCellular cytotoxicityVaccine regimensImmunological memoryNeutralizing antibodiesFollow-upFilovirus vaccinesRe-exposureReactogenicityHemorrhagic feverVaccineMultiple filovirusesHealth priorityCD4 downregulation precedes Env expression and protects HIV-1-infected cells from ADCC mediated by non-neutralizing antibodies
Richard J, Sannier G, Zhu L, Prévost J, Marchitto L, Benlarbi M, Beaudoin-Bussières G, Kim H, Sun Y, Chatterjee D, Medjahed H, Bourassa C, Delgado G, Dubé M, Kirchhoff F, Hahn B, Kumar P, Kaufmann D, Finzi A. CD4 downregulation precedes Env expression and protects HIV-1-infected cells from ADCC mediated by non-neutralizing antibodies. MBio 2024, 15: e01827-24. PMID: 39373535, PMCID: PMC11559134, DOI: 10.1128/mbio.01827-24.Peer-Reviewed Original ResearchAntibody-dependent cellular cytotoxicityProductively infected cellsEnv-CD4 interactionNon-neutralizing antibodiesHIV-1CD4 downmodulationEnv expressionCellular cytotoxicityResistance to antibody-dependent cellular cytotoxicityHIV-1-infected humanized miceInfected cellsHIV-1 cure strategiesHIV-1 mRNA expressionHIV-1-infected cellsCD4+ T cellsHIV-1 envelope glycoproteinMRNA expressionADCC-mediating antibodiesNon-neutralizing AbsCell surface CD4HIV-1 isolatesImmunotherapy-based strategiesMultiparametric flow cytometryVirally infected cellsEffective immune responseA New Chimeric Antibody against the HIV-1 Fusion Inhibitory Peptide MT-C34 with a High Affinity and Fc-Mediated Cellular Cytotoxicity
Kalinichenko S, Ramadan L, Kruglova N, Balagurov K, Lukashina M, Mazurov D, Shepelev M. A New Chimeric Antibody against the HIV-1 Fusion Inhibitory Peptide MT-C34 with a High Affinity and Fc-Mediated Cellular Cytotoxicity. Biology 2024, 13: 675. PMID: 39336102, PMCID: PMC11428423, DOI: 10.3390/biology13090675.Peer-Reviewed Original ResearchCellular cytotoxicityHIV-1Chimeric antibodyInhibitors of HIV-1 entryAntibody-dependent cellular cytotoxicityHIV-1 infectionHIV-1 entryRecombinant chimeric antibodyHumanized antibody trastuzumabMouse monoclonal antibodyCXCR4 locusCD4 lymphocytesCD4 cellsParental mouse monoclonal antibodyCAR cellsGeneration of antibodiesAntibody trastuzumabMonoclonal antibodiesAntibodiesMouse hybridomasConstant regionKnock-inCellsCytotoxicityPeptideA Noncanonical CD56dimCD16dim/- NK Cell Subset Indicative of Prior Cytotoxic Activity Is Elevated in Patients with Autoantibody-Mediated Neurologic Diseases.
Yandamuri S, Filipek B, Lele N, Cohen I, Bennett J, Nowak R, Sotirchos E, Longbrake E, Mace E, O'Connor K. A Noncanonical CD56dimCD16dim/- NK Cell Subset Indicative of Prior Cytotoxic Activity Is Elevated in Patients with Autoantibody-Mediated Neurologic Diseases. The Journal Of Immunology 2024, 212: 785-800. PMID: 38251887, PMCID: PMC10932911, DOI: 10.4049/jimmunol.2300015.Peer-Reviewed Original ResearchConceptsNeuromyelitis optica spectrum disorderAb-dependent cellular cytotoxicityNK cellsMyasthenia gravisMG patientsInduced Ab-dependent cellular cytotoxicityNK cell-mediated effector functionsPeripheral blood immune cell populationsCell-mediated effector functionsNeuromyelitis optica spectrum disorder patientsBlood immune cell populationsAb-dependent cellular cytotoxicity activityNK marker CD56NK cell markersHLA-DR expressionNK cell subsetsExpression of perforinImmune cell populationsAutoimmune myasthenia gravisElevated disease burdenHLA-DRCell subsetsCellular cytotoxicityChemokine receptorsMultiparameter immunophenotypingGeneration and optimization of off-the-shelf immunotherapeutics targeting TCR-Vβ2+ T cell malignancy
Ren J, Liao X, Lewis J, Chang J, Qu R, Carlson K, Foss F, Girardi M. Generation and optimization of off-the-shelf immunotherapeutics targeting TCR-Vβ2+ T cell malignancy. Nature Communications 2024, 15: 519. PMID: 38225288, PMCID: PMC10789731, DOI: 10.1038/s41467-024-44786-2.Peer-Reviewed Original ResearchConceptsAntibody-dependent cellular cytotoxicityDonor T cellsT cellsAdeno-associated virus transductionHealthy donor T cellsHost-versus-graft reactivityEnhanced antibody-dependent cellular cytotoxicityCAR-T cellsGraft-versus-hostT cell killingT-cell malignanciesMalignant T cellsNormal T-cellT cell receptorOff-target toxicityPre-existing immunoreactivityCAR-TDisease relapseCellular cytotoxicityVirus transductionCurrent treatmentPersister killingFc engineeringB2MIn vivo
2023
MOGAD patient autoantibodies induce complement, phagocytosis, and cellular cytotoxicity
Yandamuri S, Filipek B, Obaid A, Lele N, Thurman J, Makhani N, Nowak R, Guo Y, Lucchinetti C, Flanagan E, Longbrake E, O’Connor K. MOGAD patient autoantibodies induce complement, phagocytosis, and cellular cytotoxicity. JCI Insight 2023, 8: e165373. PMID: 37097758, PMCID: PMC10393237, DOI: 10.1172/jci.insight.165373.Peer-Reviewed Original ResearchConceptsMyelin oligodendrocyte glycoprotein antibody-associated diseaseAntibody-dependent cellular phagocytosisAntibody-dependent cellular cytotoxicityComplement-dependent cytotoxicityMOG autoantibodiesPatient seraCellular cytotoxicityEffector functionsComplement activityAntibody-associated diseaseMultiple mechanismsNK cellsPatient autoantibodiesCytotoxic capacityLesion histologyCellular phagocytosisFuture relapseIgG subclassesCerebrospinal fluidAutoantibodiesCNS conditionsMOGSerumRelapseCytotoxicityTemsavir blocks the immunomodulatory activities of HIV-1 soluble gp120
Richard J, Prévost J, Bourassa C, Brassard N, Boutin M, Benlarbi M, Goyette G, Medjahed H, Gendron-Lepage G, Gaudette F, Chen H, Tolbert W, Smith A, Pazgier M, Dubé M, Clark A, Mothes W, Kaufmann D, Finzi A. Temsavir blocks the immunomodulatory activities of HIV-1 soluble gp120. Cell Chemical Biology 2023, 30: 540-552.e6. PMID: 36958337, PMCID: PMC10198848, DOI: 10.1016/j.chembiol.2023.03.003.Peer-Reviewed Original ResearchConceptsAntibody-dependent cellular cytotoxicityUninfected bystander CD4Gp120-CD4 interactionCytokine burstBystander CD4Immunomodulatory activityMultiple immune cellsHIV-1 attachment inhibitorsOverall antigenicityADCC responsesClinical benefitSoluble gp120Immune cellsCellular cytotoxicityAttachment inhibitorsCD4 interactionGp120 bindsCD4Gp120Viral entryEnvelope glycoproteinCD4 downregulationTemsavirCellsAntigenicityAblation of SYK Kinase from Expanded Primary Human NK Cells via CRISPR/Cas9 Enhances Cytotoxicity and Cytokine Production.
Dahlvang J, Dick J, Sangala J, Kennedy P, Pomeroy E, Snyder K, Moushon J, Thefaine C, Wu J, Hamilton S, Felices M, Miller J, Walcheck B, Webber B, Moriarity B, Hart G. Ablation of SYK Kinase from Expanded Primary Human NK Cells via CRISPR/Cas9 Enhances Cytotoxicity and Cytokine Production. The Journal Of Immunology 2023, 210: 1108-1122. PMID: 36881874, PMCID: PMC10073313, DOI: 10.4049/jimmunol.2200488.Peer-Reviewed Original ResearchConceptsAb-dependent cellular cytotoxicityAdaptive NK cellsPrimary human NK cellsNK cellsHuman NK cellsCytokine productionFcRγ chainSHP-1Loss of sykTarget cell conjugationNK cell phenotypeReduced cytokine productionTNF-α productionCRISPR/Cas9 systemPhosphatase SHP-1Transcription factor PLZFCell conjugationCellular cytotoxicityImmune stateCD2 expressionSyk expressionLack expressionEnhances CytotoxicityCas9 systemEnhanced cytotoxicity
2022
HIV-1 Vpu restricts Fc-mediated effector functions in vivo
Prévost J, Anand S, Rajashekar J, Zhu L, Richard J, Goyette G, Medjahed H, Gendron-Lepage G, Chen H, Chen Y, Horwitz J, Grunst M, Zolla-Pazner S, Haynes B, Burton D, Flavell R, Kirchhoff F, Hahn B, Smith A, Pazgier M, Nussenzweig M, Kumar P, Finzi A. HIV-1 Vpu restricts Fc-mediated effector functions in vivo. Cell Reports 2022, 41: 111624. PMID: 36351384, PMCID: PMC9703018, DOI: 10.1016/j.celrep.2022.111624.Peer-Reviewed Original ResearchConceptsAntibody-dependent cellular cytotoxicityEffector functionsFc-mediated effector functionsHIV-1-infected cellsWild-type virusCorrelates of protectionRV144 vaccine trialHIV-1 infectionNon-neutralizing antibodiesFc effector functionsCell surface CD4Viral envelope glycoproteinsViral loadHumanized miceHumoral responseVaccine trialsCellular cytotoxicityHIV-1 VpuVpu expressionEnvelope glycoproteinInfected cellsNnAbsVirusVpuAdministrationEngineered ACE2-Fc counters murine lethal SARS-CoV-2 infection through direct neutralization and Fc-effector activities
Chen Y, Sun L, Ullah I, Beaudoin-Bussières G, Anand SP, Hederman AP, Tolbert WD, Sherburn R, Nguyen DN, Marchitto L, Ding S, Wu D, Luo Y, Gottumukkala S, Moran S, Kumar P, Piszczek G, Mothes W, Ackerman ME, Finzi A, Uchil PD, Gonzalez FJ, Pazgier M. Engineered ACE2-Fc counters murine lethal SARS-CoV-2 infection through direct neutralization and Fc-effector activities. Science Advances 2022, 8: eabn4188. PMID: 35857504, PMCID: PMC9278865, DOI: 10.1126/sciadv.abn4188.Peer-Reviewed Original ResearchAngiotensin-converting enzyme 2Soluble angiotensin-converting enzyme 2Fc effector functionsSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) receptorLethal SARS-CoV-2 infectionK18-hACE2 mouse modelSARS-CoV-2 infectionAntibody-dependent cellular cytotoxicitySARS-CoV-2 antiviralsFc effector activityCoV-2 infectionSARS-CoV-2 variantsHalf maximal inhibitory concentrationComplement depositionACE2-FcCellular cytotoxicityEnzyme 2Mouse modelTherapeutic activityInhibitory concentrationTherapeutic settingDirect neutralizationInfectionReceptorsEffect of neutralization
2021
Modulating HIV-1 envelope glycoprotein conformation to decrease the HIV-1 reservoir
Rajashekar JK, Richard J, Beloor J, Prévost J, Anand SP, Beaudoin-Bussières G, Shan L, Herndler-Brandstetter D, Gendron-Lepage G, Medjahed H, Bourassa C, Gaudette F, Ullah I, Symmes K, Peric A, Lindemuth E, Bibollet-Ruche F, Park J, Chen HC, Kaufmann DE, Hahn BH, Sodroski J, Pazgier M, Flavell RA, Smith AB, Finzi A, Kumar P. Modulating HIV-1 envelope glycoprotein conformation to decrease the HIV-1 reservoir. Cell Host & Microbe 2021, 29: 904-916.e6. PMID: 34019804, PMCID: PMC8214472, DOI: 10.1016/j.chom.2021.04.014.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, NeutralizingAntibody-Dependent Cell CytotoxicityAntiviral AgentsCD4 AntigensCD4-Positive T-LymphocytesCell Lineenv Gene Products, Human Immunodeficiency VirusEpitopesFemaleGlycoproteinsHEK293 CellsHIV InfectionsHIV-1HumansImmunoglobulin Fc FragmentsKiller Cells, NaturalMaleMiceMice, SCIDModels, AnimalProtein ConformationVirus ReplicationConceptsAntibody-dependent cellular cytotoxicityHIV-1 reservoirFc effector functionsViral reboundHumanized miceHIV-1HIV-1-infected individualsHIV-1-infected cellsAutologous HIV-1Natural killer cellsCD4-mimetic compoundsHIV-1 replicationSmall CD4-mimetic compoundsART interruptionFunctional cureNK cellsKiller cellsCellular cytotoxicityTherapeutic utilityInfected individualsCD4mcVirus reservoirMiceViral envelopeAntibody recognition
2018
Chapter 4 Nanocytotoxicity
Zanganeh S, Spitler R, Erfanzadeh M, Ho J, Aieneravaie M. Chapter 4 Nanocytotoxicity. 2018, 105-114. DOI: 10.1016/b978-0-08-101925-2.00012-7.Peer-Reviewed Original Research
2016
SYD985, a Novel Duocarmycin-Based HER2-Targeting Antibody–Drug Conjugate, Shows Antitumor Activity in Uterine Serous Carcinoma with HER2/Neu Expression
Black J, Menderes G, Bellone S, Schwab CL, Bonazzoli E, Ferrari F, Predolini F, De Haydu C, Cocco E, Buza N, Hui P, Wong S, Lopez S, Ratner E, Silasi DA, Azodi M, Litkouhi B, Schwartz PE, Goedings P, Beusker PH, van der Lee MM, Timmers CM, Dokter WH, Santin AD. SYD985, a Novel Duocarmycin-Based HER2-Targeting Antibody–Drug Conjugate, Shows Antitumor Activity in Uterine Serous Carcinoma with HER2/Neu Expression. Molecular Cancer Therapeutics 2016, 15: 1900-1909. PMID: 27256376, DOI: 10.1158/1535-7163.mct-16-0163.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAnimalsAntibody-Dependent Cell CytotoxicityAntineoplastic AgentsBystander EffectCathepsin BCell Line, TumorCell SurvivalClass I Phosphatidylinositol 3-KinasesCystadenocarcinoma, SerousDisease Models, AnimalDuocarmycinsFemaleGene ExpressionHumansImmunoconjugatesIndolesMiceMiddle AgedMutationPhosphatidylinositol 3-KinasesPyrrolidinonesReceptor, ErbB-2Survival AnalysisUterine NeoplasmsXenograft Model Antitumor AssaysConceptsUterine serous carcinomaAntibody-dependent cellular cytotoxicityHER2/neu expressionAntibody-drug conjugatesT-DM1Neu expressionHER2-targeting antibody-drug conjugateNovel antibody-drug conjugateNovel HER2-targeting antibody-drug conjugatePrimary USC cell linesHigh HER2 expressionHER2/neu oncogeneHER2/neuMouse xenograft modelUSC cell linesFlow cytometry assayEndometrial cancerSerous carcinomaHER2 expressionTrastuzumab emtansineClinical studiesCellular cytotoxicitySYD985Aggressive formExpress HER2
2014
Patients with Griscelli syndrome and normal pigmentation identify RAB27A mutations that selectively disrupt MUNC13-4 binding
Cetica V, Hackmann Y, Grieve S, Sieni E, Ciambotti B, Coniglio M, Pende D, Gilmour K, Romagnoli P, Griffiths G, Aricò M. Patients with Griscelli syndrome and normal pigmentation identify RAB27A mutations that selectively disrupt MUNC13-4 binding. Journal Of Allergy And Clinical Immunology 2014, 135: 1310-1318.e1. PMID: 25312756, PMCID: PMC4418747, DOI: 10.1016/j.jaci.2014.08.039.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAdolescentAlbinismCase-Control StudiesCell DegranulationCell LineChildChild, PreschoolCohort StudiesCytotoxicity, ImmunologicDNA Mutational AnalysisFemaleGene ExpressionGenetic MarkersHumansInfantLymphohistiocytosis, HemophagocyticMaleMembrane ProteinsModels, MolecularMutationPerforinPhenotypeProtein BindingProtein Conformationrab GTP-Binding Proteinsrab27 GTP-Binding ProteinsSkin PigmentationConceptsFamilial hemophagocytic lymphohistiocytosisCellular cytotoxicityHematopoietic stem cell transplantationMunc13-4Griscelli syndrome type 2FHL-related genesInteraction of Rab27aStem cell transplantationPigment dilutionAbsence of albinismNormal pigmentationHemophagocytic lymphohistiocytosisCell transplantationClinical evidenceBiallelic mutationsRAB27A mutationsFatal disorderGenetic diagnosisOculocutaneous albinismPatientsGriscelli syndromeAffecting pigmentationType 2Rab27aMutation analysisDiagnosing XLP1 in patients with hemophagocytic lymphohistiocytosis
Meazza R, Tuberosa C, Cetica V, Falco M, Parolini S, Grieve S, Griffiths G, Sieni E, Marcenaro S, Micalizzi C, Montin D, Fagioli F, Moretta A, Mingari M, Moretta L, Notarangelo L, Bottino C, Aricò M, Pende D. Diagnosing XLP1 in patients with hemophagocytic lymphohistiocytosis. Journal Of Allergy And Clinical Immunology 2014, 134: 1381-1387.e7. PMID: 24985396, PMCID: PMC7611500, DOI: 10.1016/j.jaci.2014.04.043.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAntigens, CDChildChild, PreschoolFemaleHumansInfantIntracellular Signaling Peptides and ProteinsKiller Cells, NaturalLeukocytes, MononuclearLymphohistiocytosis, HemophagocyticLymphoproliferative DisordersMaleMutationReceptors, ImmunologicSignaling Lymphocytic Activation Molecule Associated ProteinSignaling Lymphocytic Activation Molecule FamilyYoung AdultConceptsX-linked lymphoproliferative disease 1Signaling lymphocytic activation molecule-associated proteinSignaling lymphocytic activation molecule-associated protein expressionHemophagocytic lymphohistiocytosisSH2D1A mutationsNatural killerNK cellsSAP expressionPeripheral blood NK cellsMutation analysisRange of healthy controlsBlood NK cellsNK cell levelsImpaired natural killerCohort of patientsEBV-infected cellsDefective killingCellular cytotoxicityHealthy controlsDiagnostic evaluationLife-threateningSH2D1ADisease 1Prompt identificationPatients
2012
Antibody targeting of anaplastic lymphoma kinase induces cytotoxicity of human neuroblastoma
Carpenter EL, Haglund EA, Mace EM, Deng D, Martinez D, Wood AC, Chow AK, Weiser DA, Belcastro LT, Winter C, Bresler SC, Asgharzadeh S, Seeger R, Zhao H, Guo R, Christensen J, Orange J, Pawel B, Lemmon M, Mossé Y. Antibody targeting of anaplastic lymphoma kinase induces cytotoxicity of human neuroblastoma. Oncogene 2012, 31: 4859-4867. PMID: 22266870, PMCID: PMC3730824, DOI: 10.1038/onc.2011.647.Peer-Reviewed Original ResearchMeSH KeywordsAnaplastic Lymphoma KinaseAntibodies, MonoclonalAntigens, NeoplasmCell DeathCell Line, TumorCell ProliferationCrizotinibHumansMutationNeuroblastomaPhosphorylationProtein Kinase InhibitorsProtein-Tyrosine KinasesProto-Oncogene Proteins c-metPyrazolesPyridinesReceptor Protein-Tyrosine KinasesSignal TransductionConceptsAnaplastic lymphoma kinaseLymphoma kinaseHuman neuroblastomaSmall molecule tyrosine kinase inhibitorsAntibody-dependent cellular cytotoxicityReceptor tyrosine kinasesDevastating pediatric cancerSympathetic nervous systemALK inhibitor crizotinibComplementary therapeutic approachALK-positive tumorsPromising therapeutic strategyTyrosine kinase inhibitorsAntibody-induced growth inhibitionCell linesTractable therapeutic targetWild-type ALKTyrosine kinaseALK aberrationsNeuroblastoma patientsLung cancerALK mutationsInhibitor crizotinibCellular cytotoxicityALK antibody
2011
Trop-2 Overexpression in Poorly Differentiated Endometrial Endometrioid Carcinoma Implications for Immunotherapy With hRS7, a Humanized Anti-Trop-2 Monoclonal Antibody
Bignotti E, Ravaggi A, Romani C, Falchetti M, Lonardi S, Facchetti F, Pecorelli S, Varughese J, Cocco E, Bellone S, Schwartz PE, Rutherford TJ, Santin AD. Trop-2 Overexpression in Poorly Differentiated Endometrial Endometrioid Carcinoma Implications for Immunotherapy With hRS7, a Humanized Anti-Trop-2 Monoclonal Antibody. International Journal Of Gynecological Cancer 2011, 21: 1613-1621. PMID: 21892093, PMCID: PMC3233648, DOI: 10.1097/igc.0b013e318228f6da.Peer-Reviewed Original ResearchMeSH KeywordsAntibodies, MonoclonalAntibody-Dependent Cell CytotoxicityAntigens, NeoplasmCarcinoma, EndometrioidCell Adhesion MoleculesCell DifferentiationCell Line, TumorComplement System ProteinsEndometrial NeoplasmsFemaleFlow CytometryHumansImmunization, PassiveImmunoglobulin GImmunohistochemistryRNA, MessengerConceptsEndometrial endometrioid carcinomaNormal endometrial controlsTrop-2 expressionEEC cell linesAntibody-dependent cellular cytotoxicityReal-time polymerase chain reactionQuantitative real-time polymerase chain reactionEndometrioid carcinomaPolymerase chain reactionCellular cytotoxicityTrop-2Anti-Trop-2 antibodyCell linesTherapeutic agentsCr-release assaysTrop-2 overexpressionGrade 3 tumorsStandard treatment modalityChain reactionNovel therapeutic agentsCell surface markersEndometrial controlTreatment modalitiesPrimary cell linesEEC samplesUterine and ovarian carcinosarcomas overexpressing Trop-2 are sensitive to hRS7, a humanized anti-Trop-2 antibody
Raji R, Guzzo F, Carrara L, Varughese J, Cocco E, Bellone S, Betti M, Todeschini P, Gasparrini S, Ratner E, Silasi DA, Azodi M, Schwartz P, Rutherford TJ, Buza N, Pecorelli S, Santin AD. Uterine and ovarian carcinosarcomas overexpressing Trop-2 are sensitive to hRS7, a humanized anti-Trop-2 antibody. Journal Of Experimental & Clinical Cancer Research 2011, 30: 106. PMID: 22075385, PMCID: PMC3224774, DOI: 10.1186/1756-9966-30-106.Peer-Reviewed Original ResearchConceptsAntibody-dependent cellular cytotoxicityAnti-Trop-2 antibodyTrop-2Cell linesEffective treatment optionChromium release assaysComplement-dependent cytotoxicityCarcinosarcoma cell lineCell surface markersOvarian carcinosarcomaTreatment optionsControl antibodyHRS7Cellular cytotoxicityHigher positivityTherapeutic strategiesHuman uterineTumor tissueFlow cytometryImmunohistochemistryRT-PCRSurface expressionAntibodiesHuman IgGCarcinosarcomaFamilial hemophagocytic lymphohistiocytosis: a model for understanding the human machinery of cellular cytotoxicity
Sieni E, Cetica V, Mastrodicasa E, Pende D, Moretta L, Griffiths G, Aricò M. Familial hemophagocytic lymphohistiocytosis: a model for understanding the human machinery of cellular cytotoxicity. Cellular And Molecular Life Sciences 2011, 69: 29-40. PMID: 21990010, PMCID: PMC11114696, DOI: 10.1007/s00018-011-0835-y.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsChediak-Higashi SyndromeCytoplasmic GranulesCytotoxicity, ImmunologicHermanski-Pudlak SyndromeHumansImmunologic Deficiency SyndromesKiller Cells, NaturalLymphocyte SubsetsLymphohistiocytosis, HemophagocyticLymphoproliferative DisordersMacrophage Activation SyndromeMembrane ProteinsMiceMunc18 ProteinsNatural Killer T-CellsPerforinPiebaldismPore Forming Cytotoxic ProteinsPrimary Immunodeficiency DiseasesQa-SNARE ProteinsT-Lymphocytes, CytotoxicConceptsCellular cytotoxicityGenetic immune deficienciesCellular cytotoxic mechanismsCytotoxic T lymphocytesNatural killer cellsKill infected cellsFamilial hemophagocytic lymphohistiocytosisInherited human disordersNKT cellsHemophagocytic lymphohistiocytosisProspective trialsEffector cellsImmune deficiencyKiller cellsT lymphocytesClinical pictureRare diseaseClinical syndromeTherapeutic approachesImprove outcomesGenetic subsetsGenetic studiesCytotoxic mechanismInfected cellsHuman disorders
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