2021
Nonsurgical treatment of skin cancer with local delivery of bioadhesive nanoparticles
Hu JK, Suh HW, Qureshi M, Lewis JM, Yaqoob S, Moscato ZM, Griff S, Lee AK, Yin ES, Saltzman WM, Girardi M. Nonsurgical treatment of skin cancer with local delivery of bioadhesive nanoparticles. Proceedings Of The National Academy Of Sciences Of The United States Of America 2021, 118: e2020575118. PMID: 33526595, PMCID: PMC7896333, DOI: 10.1073/pnas.2020575118.Peer-Reviewed Original ResearchConceptsSquamous cell carcinomaNonsurgical treatmentSkin cancerTumor cell surfaceIntratumoral drug deliveryHistologic cureCutaneous malignanciesSurgical excisionTherapeutic standardTumor burdenTumor immunotherapyTumor injectionCommon malignancyCell carcinomaSCC tumorsNonsurgical alternativeTherapeutic efficacyD postinjectionNanoparticle drug delivery systemsChemotherapeutic agentsSuperficial tumorsTumorsLocal deliveryEnhanced survivalPercutaneous delivery
2019
Novel Protocol for Generating Physiologic Immunogenic Dendritic Cells.
Ventura A, Vassall A, Yurter A, Robinson E, Filler R, Hanlon D, Meeth K, Ezaldein H, Girardi M, Sobolev O, Bosenberg MW, Edelson RL. Novel Protocol for Generating Physiologic Immunogenic Dendritic Cells. Journal Of Visualized Experiments 2019 PMID: 31157760, DOI: 10.3791/59370.Peer-Reviewed Original ResearchConceptsCutaneous T-cell lymphomaDendritic cellsCellular vaccinesClinical efficacyAnti-tumor T cell immunityVivo anti-tumor responsesMonocyte-derived dendritic cellsTumor cellsSyngeneic mouse tumor modelsImmunogenic dendritic cellsAnti-cancer immunityT cell immunityAnti-tumor responseHuman dendritic cellsT-cell lymphomaAnti-tumor effectsKey mechanistic driversApoptotic tumor cellsMouse tumor modelsCell immunitySafety profileCancer immunotherapyCell lymphomaMouse modelBlood samples
2018
Extracorporeal Photochemotherapy Drives Monocyte-to-Dendritic Cell Maturation to Induce Anti-Cancer Immunity
Ventura A, Vassall A, Robinson E, Filler R, Hanlon D, Meeth K, Ezaldein H, Girardi M, Sobolev O, Bosenberg MW, Edelson RL. Extracorporeal Photochemotherapy Drives Monocyte-to-Dendritic Cell Maturation to Induce Anti-Cancer Immunity. Cancer Research 2018, 78: canres.0171.2018. PMID: 29764863, DOI: 10.1158/0008-5472.can-18-0171.Peer-Reviewed Original ResearchConceptsT cellsT cell antitumor immunityTumor-specific T cellsTumor cellsEffective immunotherapeutic agentFavorable safety profileResponder T cellsDendritic cell differentiationTumor-challenged miceImmunogenic cell deathSelective antitumor effectApoptotic tumor cellsPotential therapeutic applicabilityProcessing/presentationAntimelanoma immunityHealthy DCsImmunogenic malignanciesAntitumor immunityCellular vaccinesImmunotherapeutic effectsAdditional malignanciesImmunotherapeutic agentsSafety profileCancer immunotherapyTumor antigens
2009
CD27 is a thymic determinant of the balance between interferon-γ- and interleukin 17–producing γδ T cell subsets
Ribot JC, deBarros A, Pang DJ, Neves JF, Peperzak V, Roberts SJ, Girardi M, Borst J, Hayday AC, Pennington DJ, Silva-Santos B. CD27 is a thymic determinant of the balance between interferon-γ- and interleukin 17–producing γδ T cell subsets. Nature Immunology 2009, 10: 427-436. PMID: 19270712, PMCID: PMC4167721, DOI: 10.1038/ni.1717.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCD27 LigandCells, CulturedInterferon-gammaInterleukin-17Lymphoid Progenitor CellsLymphotoxin beta ReceptorMalaria, CerebralMiceMice, Inbred C57BLPlasmodium bergheiReceptors, Antigen, T-Cell, gamma-deltaThymus GlandT-Lymphocyte SubsetsTumor Necrosis Factor Receptor Superfamily, Member 7
2007
Promotion of Hras-induced squamous carcinomas by a polymorphic variant of the Patched gene in FVB mice
Wakabayashi Y, Mao JH, Brown K, Girardi M, Balmain A. Promotion of Hras-induced squamous carcinomas by a polymorphic variant of the Patched gene in FVB mice. Nature 2007, 445: 761-765. PMID: 17230190, DOI: 10.1038/nature05489.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsApoptosisCarcinoma, Squamous CellCell LineCell Transformation, NeoplasticCrosses, GeneticFemaleGene Expression Regulation, NeoplasticGenes, rasHSP40 Heat-Shock ProteinsHumansKruppel-Like Transcription FactorsMaleMiceMice, Inbred C57BLMice, TransgenicMolecular Sequence DataPatched ReceptorsPatched-1 ReceptorPolymorphism, GeneticRas ProteinsReceptors, Cell SurfaceZinc Finger Protein Gli2ConceptsSquamous carcinomaTumor suppressor geneFVB/N miceSonic hedgehogSuppressor geneFVB/N strainBasal cell carcinomaPTCH geneSame target cellsCell lineage commitmentPatched geneHuman patched geneHost genetic backgroundClassical tumor suppressor geneCell carcinomaPtch alleleFVB miceN miceCarcinogen exposureC57BL/6 strainTumor typesLineage commitmentMouse homologueHybrid miceGenetic basis
2005
Sustained localized expression of ligand for the activating NKG2D receptor impairs natural cytotoxicity in vivo and reduces tumor immunosurveillance
Oppenheim DE, Roberts SJ, Clarke SL, Filler R, Lewis JM, Tigelaar RE, Girardi M, Hayday AC. Sustained localized expression of ligand for the activating NKG2D receptor impairs natural cytotoxicity in vivo and reduces tumor immunosurveillance. Nature Immunology 2005, 6: 928-937. PMID: 16116470, DOI: 10.1038/ni1239.Peer-Reviewed Original ResearchMeSH Keywords9,10-Dimethyl-1,2-benzanthraceneAnimalsCarcinomaCell Line, TumorDisease SusceptibilityDown-RegulationFemaleImmunologic SurveillanceKiller Cells, NaturalLigandsMaleMembrane ProteinsMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicNK Cell Lectin-Like Receptor Subfamily KPapillomaReceptors, ImmunologicReceptors, Natural Killer CellSkin NeoplasmsTetradecanoylphorbol AcetateT-LymphocytesTumor BurdenConceptsNKG2D downregulationNK cell-mediated cytotoxicityNatural killer cellsCell-mediated cytotoxicityInnate immune activationT cell defectsNKG2D engagementNatural cytotoxicityKiller cellsImmune activationReceptor NKG2DTumor immunosurveillanceCutaneous carcinogenesisTumor surveillanceT cellsReversible defectsRAE-1Normal epitheliumLigand expressionTumor resistanceCell defectsSustained expressionNKG2DImmunosurveillanceDownregulation
2004
Characterizing the Protective Component of the αβ T Cell Response to Transplantable Squamous Cell Carcinoma
Girardi M, Oppenheim D, Glusac EJ, Filler R, Balmain A, Tigelaar RE, Hayday AC. Characterizing the Protective Component of the αβ T Cell Response to Transplantable Squamous Cell Carcinoma. Journal Of Investigative Dermatology 2004, 122: 699-706. PMID: 15086556, DOI: 10.1111/j.0022-202x.2004.22342.x.Peer-Reviewed Original ResearchConceptsT cell responsesImmune responseCell responsesProtective anti-tumor effectTransplantable squamous cell carcinomaT cell-deficient miceAlphabeta T cell responsesCell-deficient miceT cell activityCellular immune responsesSquamous cell carcinomaΑβ T cell responsesSquamous cell carcinoma linesAlphabeta T cellsAnti-tumor effectsNK receptorsCell carcinomaT cellsFocal necrosesRAE-1Protective potentialTumor growthProtective responseStromal bedCell activity
2003
γδ T Cells Provide an Early Source of Interferon γ in Tumor Immunity
Gao Y, Yang W, Pan M, Scully E, Girardi M, Augenlicht LH, Craft J, Yin Z. γδ T Cells Provide an Early Source of Interferon γ in Tumor Immunity. Journal Of Experimental Medicine 2003, 198: 433-442. PMID: 12900519, PMCID: PMC2194096, DOI: 10.1084/jem.20030584.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsImmunity, CellularInterferon-gammaInterleukin-12Lymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutNeoplasm TransplantationNeoplasms, ExperimentalReceptors, Antigen, T-Cell, alpha-betaReceptors, Antigen, T-Cell, gamma-deltaT-Lymphocyte SubsetsTransplantation ChimeraTumor Cells, CulturedConceptsGammadelta T cellsAlphabeta T cellsT cellsTumor immunityIFN-gammaHigh incidenceGammadelta T cell-deficient miceImpaired IFN-gamma productionT cell-deficient miceTumor developmentCell-deficient miceBone marrow chimerasΓδ T cellsIFN-gamma productionSite of tumorT cell repertoireWild-type miceChemical carcinogen methylcholanthreneMelanoma cell line B16B16 melanoma cellsTumor lysateCarcinogen methylcholanthreneTumor immunosurveillanceInterferon γSuch miceAnti‐inflammatory effects in the skin of thymosin‐β4 splice‐variants
Girardi M, Sherling MA, Filler RB, Shires J, Theodoridis E, Hayday AC, Tigelaar RE. Anti‐inflammatory effects in the skin of thymosin‐β4 splice‐variants. Immunology 2003, 109: 1-7. PMID: 12709011, PMCID: PMC1782938, DOI: 10.1046/j.1365-2567.2003.01616.x.Peer-Reviewed Original ResearchConceptsDendritic epidermal T cellsContact dermatitisAnti-inflammatory effectsEpidermal T cellsAnti-inflammatory propertiesIrritant contact dermatitisAllergic contact dermatitisAnti-inflammatory activityT cell receptorNeutrophil infiltrationNeutrophilic infiltrationCutaneous inflammationLocal inflammationLymphoid tissueT cellsMurine skinCellular activationInflammationDermatitisThymosin β4SkinIELInfiltrationUnknown bioactivitiesGene expression
2002
Resident Skin-specific γδ T Cells Provide Local, Nonredundant Regulation of Cutaneous Inflammation
Girardi M, Lewis J, Glusac E, Filler RB, Geng L, Hayday AC, Tigelaar RE. Resident Skin-specific γδ T Cells Provide Local, Nonredundant Regulation of Cutaneous Inflammation. Journal Of Experimental Medicine 2002, 195: 855-867. PMID: 11927630, PMCID: PMC2193718, DOI: 10.1084/jem.20012000.Peer-Reviewed Original ResearchConceptsT cell receptorEpidermal T cellsT cellsIrritant dermatitisGammadelta T-cell receptorT cell-mediated inflammationCell-mediated inflammationSystemic inflammatory reactionIrritant contact dermatitis reactionsΓδ T cellsGammadelta T cellsContact dermatitis reactionsCutaneous inflammationIEL subsetsChronic dermatitisFunctional impairmentInflammatory reactionDermatitis reactionsEpithelial interfaceCell subpopulationsCell receptorMiceMouse strainsDermatitisSingle autosomal recessive gene
2001
Regulation of Cutaneous Malignancy by γδ T Cells
Girardi M, Oppenheim D, Steele C, Lewis J, Glusac E, Filler R, Hobby P, Sutton B, Tigelaar R, Hayday A. Regulation of Cutaneous Malignancy by γδ T Cells. Science 2001, 294: 605-609. PMID: 11567106, DOI: 10.1126/science.1063916.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsCarcinogensCell LineCytotoxicity, ImmunologicDimerizationEpidermisEpithelial CellsHistocompatibility Antigens Class IHumansImmunologic SurveillanceLigandsMembrane ProteinsMiceMice, Inbred C57BLMinor Histocompatibility AntigensMolecular Sequence DataNK Cell Lectin-Like Receptor Subfamily KProtein ConformationProtein FoldingReceptors, Antigen, T-Cell, alpha-betaReceptors, Antigen, T-Cell, gamma-deltaReceptors, ImmunologicReceptors, Natural Killer CellRecombinant Fusion ProteinsReverse Transcriptase Polymerase Chain ReactionSkin NeoplasmsT-Lymphocyte SubsetsConceptsT cellsGammadelta cellsLocal T cellsNatural killer cellsΓδ T cellsGammadelta T cellsCytolytic T cellsSkin carcinoma cellsNKG2D engagementMultiple regimensKiller cellsCutaneous malignanciesCutaneous carcinogenesisEpithelial malignanciesRAE-1Human MICAMalignancyCarcinoma cellsSkin cellsCellsNKG2DRegimensMiceEpitheliumCarcinogenesis
1995
α β and γ δ T cells can share a late common precursor
Dudley E, Girardi M, Owen M, Hayday A. α β and γ δ T cells can share a late common precursor. Current Biology 1995, 5: 659-669. PMID: 7552177, DOI: 10.1016/s0960-9822(95)00131-x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsBase SequenceCell DifferentiationDendritic CellsDNA NucleotidyltransferasesGene Rearrangement, T-LymphocyteHematopoiesisHematopoietic Stem CellsMiceMice, Inbred C57BLMolecular Sequence DataPolymerase Chain ReactionPolymorphism, Restriction Fragment LengthReceptors, Antigen, T-Cell, alpha-betaReceptors, Antigen, T-Cell, gamma-deltaStochastic ProcessesT-Lymphocyte SubsetsVDJ RecombinasesConceptsDelta geneSuccessful rearrangementLineage-determining factorsT cell receptorGene rearrangement processTCR-alpha gene rearrangementsAlpha gene rearrangementsTCR beta locusVertebrate developmentTCR delta geneAlpha betaSeparate lineagesTCR delta locusProductive rearrangementsDelta gene segmentsDelta locusBeta locusPolypeptide chainIndividual thymocytesGenesGamma geneT cell differentiationGene segmentsFragment length polymorphism techniqueCommon precursorSpecific Suppression of Lupus-Like Graft-Versus-Host Disease Using Extracorporeal Photochemical Attenuation of Effector Lymphocytes
Girardi M, Herreid P, Tigelaar R. Specific Suppression of Lupus-Like Graft-Versus-Host Disease Using Extracorporeal Photochemical Attenuation of Effector Lymphocytes. Journal Of Investigative Dermatology 1995, 104: 177-182. PMID: 7829872, DOI: 10.1111/1523-1747.ep12612741.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntibodies, AntinuclearAscitesAutoimmune DiseasesDisease Models, AnimalFemaleGlomerulonephritisGraft vs Host DiseaseGraft vs Host ReactionImmunotherapy, AdoptiveKidneyLupus Erythematosus, SystemicMiceMice, Inbred C3HMice, Inbred C57BLMice, Inbred DBAPUVA TherapyT-LymphocytesVaccinationConceptsSystemic lupus erythematosus-like diseaseB6D2F1 recipientsDisease initiationD2 cellsAntinuclear antibody titerLupus-like graftProgression of graftVersus Host DiseaseSystemic lupus erythematosusC3H/HeJ xDBA/2 splenocytesHost diseaseLupus erythematosusEffector lymphocytesClinical manifestationsClinical parametersHistologic evidenceAntibody titersKidney diseaseAscites formationB6D2F1 miceInterleukin-2T cellsC57BL/6 xComplex antigens