2018
Both HIV-Infected and Uninfected Cells Express TRAILshort, Which Confers TRAIL Resistance upon Bystander Cells within the Microenvironment
Nie Z, Aboulnasr F, Natesampillai S, Burke S, Krogman A, Bren G, Chung T, Anderson J, Smart M, Katzmann D, Rajagopalan G, Cummins N, Badley A. Both HIV-Infected and Uninfected Cells Express TRAILshort, Which Confers TRAIL Resistance upon Bystander Cells within the Microenvironment. The Journal Of Immunology 2018, 200: 1110-1123. PMID: 29263214, PMCID: PMC5808399, DOI: 10.4049/jimmunol.1701113.Peer-Reviewed Original ResearchConceptsTRAIL resistanceBystander cellsNeighboring bystander cellsUninfected bystander cellsType I IFNsOvercoming TRAIL ResistanceTRAIL receptor 1Apoptosis-inducing ligandHIV diseaseTLR9 agonistsImmune eliminationReceptor axisTRAILshortI IFNsSpecific AbsHIVReceptor 1Tumor cellsTRAIL sensitivityNormal cellsDominant negative ligandCellsSplice variantsMicroenvironmentKilling
2015
Superantigen-Producing Staphylococcus aureus Elicits Systemic Immune Activation in a Murine Wound Colonization Model
Kim C, Karau M, Greenwood-Quaintance K, Tilahun A, Krogman A, David C, Pritt B, Patel R, Rajagopalan G. Superantigen-Producing Staphylococcus aureus Elicits Systemic Immune Activation in a Murine Wound Colonization Model. Toxins 2015, 7: 5308-5319. PMID: 26670252, PMCID: PMC4690136, DOI: 10.3390/toxins7124886.Peer-Reviewed Original ResearchConceptsSystemic immune activationImmune activationT cellsS. aureusSerum IL-17 levelsSystemic immunologic effectsIL-17 levelsSpleens of miceWound infection modelImmunologic effectsInflammatory changesHLA-DR3Wound infectionCommon causeTransgenic miceUninfected woundsDay 8Immune systemClinical implicationsInfection modelMiceSkin woundsWoundsMicrobial challengeStaphylococcus aureusA Central Role for HLA-DR3 in Anti-Smith Antibody Responses and Glomerulonephritis in a Transgenic Mouse Model of Spontaneous Lupus
Chowdhary VR, Dai C, Tilahun AY, Hanson JA, Smart MK, Grande JP, Rajagopalan G, Fu SM, David CS. A Central Role for HLA-DR3 in Anti-Smith Antibody Responses and Glomerulonephritis in a Transgenic Mouse Model of Spontaneous Lupus. The Journal Of Immunology 2015, 195: 4660-4667. PMID: 26475924, PMCID: PMC5292932, DOI: 10.4049/jimmunol.1501073.Peer-Reviewed Original ResearchConceptsHLA-DR3NZM2328 miceClass IIMouse modelEndogenous MHC class IIAnti-dsDNA titersWire-loop lesionsSystemic lupus erythematosusSpecific HLA allelesMHC class IITransgenic mouse modelAnti-Sm AbsLupus erythematosusSevere proteinuriaAutoimmune responseHLA-DR2Lymphoid aggregatesAntibody responseHLA-DR3 moleculesHistological scoresT cellsImmune responseSpontaneous lupusHLA allelesHuman studiesSuperantigens produced by catheter-associated Staphylococcus aureus elicit systemic inflammatory disease in the absence of bacteremia
Chung J, Greenwood-Quaintance K, Karau MJ, Tilahun A, Khaleghi SR, Chowdhary VR, David CS, Patel R, Rajagopalan G. Superantigens produced by catheter-associated Staphylococcus aureus elicit systemic inflammatory disease in the absence of bacteremia. Journal Of Leukocyte Biology 2015, 98: 271-281. PMID: 25979434, PMCID: PMC4501677, DOI: 10.1189/jlb.4a1214-577rr.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCatheter-Related InfectionsCatheters, IndwellingCD4-Positive T-LymphocytesEnterotoxinsGene DeletionHistocompatibility AntigensHumansKidneyLiverLungLymphocyte ActivationMiceMice, TransgenicReceptors, Antigen, T-Cell, alpha-betaSpleenStaphylococcal InfectionsStaphylococcus aureusSuperantigensConceptsS. aureusHLA-DR3 transgenic miceLong intravenous catheterSystemic immune activationSerum cytokine levelsSystemic inflammatory diseaseAbsence of bacteremiaMHC class II moleculesInvasive staphylococcal diseaseToxigenic S. aureusClinical S. aureus isolatesS. aureus isolatesClass II moleculesIsogenic S. aureusCytokine levelsHLA-DR3Immune activationInflammatory diseasesIntravenous cathetersStaphylococcal diseaseRole of SAgsDevice-associated infectionsT cellsClinical consequencesForeign body
2012
Chronic Exposure to Staphylococcal Superantigen Elicits a Systemic Inflammatory Disease Mimicking Lupus
Chowdhary VR, Tilahun AY, Clark CR, Grande JP, Rajagopalan G. Chronic Exposure to Staphylococcal Superantigen Elicits a Systemic Inflammatory Disease Mimicking Lupus. The Journal Of Immunology 2012, 189: 2054-2062. PMID: 22798666, PMCID: PMC3462343, DOI: 10.4049/jimmunol.1201097.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAutoantibodiesAutoantigensAutoimmune DiseasesCD28 AntigensCD4-Positive T-LymphocytesEnzyme-Linked Immunosorbent AssayFlow CytometryFluorescent Antibody TechniqueHLA-DQ AntigensHumansInfusions, SubcutaneousLupus Erythematosus, SystemicMiceMice, TransgenicStaphylococcus aureusSuperantigensConceptsSystemic lupus erythematosusT cellsChronic exposureStaphylococcal enterotoxin BLupus erythematosusMouse MHC class II moleculesHLA-DQ8 transgenic miceMultisystem autoimmune inflammatory diseaseEnterotoxin BHLA-DQ8 miceAutoimmune inflammatory diseaseMHC class II moleculesTh1-type cytokinesMini-osmotic pumpsMononuclear cell infiltrationAnti-nuclear AbsClass II moleculesAbsence of diseaseChronic nasalIL-12Inflammatory infiltrateAutoimmune diseasesCell infiltrationInflammatory diseasesPathogenic role
2011
Human Leukocyte Antigen Class II Transgenic Mouse Model Unmasks the Significant Extrahepatic Pathology in Toxic Shock Syndrome
Tilahun A, Marietta E, Wu T, Patel R, David C, Rajagopalan G. Human Leukocyte Antigen Class II Transgenic Mouse Model Unmasks the Significant Extrahepatic Pathology in Toxic Shock Syndrome. American Journal Of Pathology 2011, 178: 2760-2773. PMID: 21641398, PMCID: PMC3124354, DOI: 10.1016/j.ajpath.2011.02.033.Peer-Reviewed Original ResearchConceptsToxic shock syndromeShock syndromeTransgenic miceSmall intestineHLA-DR3 transgenic miceHLA class II moleculesMultiple organ inflammationPotent T cell activatorsKey pathogenic eventClass II moleculesT cell activatorsGut dysfunctionKawasaki diseaseLiver failureHeavy infiltrationHigh morbidityD-GalN.Pathologic changesT lymphocytesExtrahepatic pathologyPathogenic eventsAbsorptive functionD-galactosamineSensitization modelMouse strains
2007
Distinct local immunogenic stimuli dictate differential requirements for CD4+ and CD8+ T cell subsets in the pathogenesis of spontaneous autoimmune diabetes
Rajagopalan G, Mangalam A, Sen M, Kudva Y, David C. Distinct local immunogenic stimuli dictate differential requirements for CD4+ and CD8+ T cell subsets in the pathogenesis of spontaneous autoimmune diabetes. Autoimmunity 2007, 40: 489-496. PMID: 17966038, DOI: 10.1080/08916930701649836.Peer-Reviewed Original ResearchConceptsIncidence of diabetesPathogenesis of T1DRat insulin promoterTransgenic mouse modelMouse modelHLA-DQ8 transgenic miceMurine type 1 diabetesDouble transgenic mouse modelMHC class II associationsLocal inflammatory stimuliSpontaneous autoimmune diabetesT cell subsetsClass II associationsType 1 diabetesAutoimmune diabetesImmunogenic stimulusProinflammatory cytokinesCell subsetsCostimulatory moleculesTNF-alphaT cellsInflammatory stimuliDiabetesTransgenic miceCD4
2006
Acute Systemic Immune Activation following Conjunctival Exposure to Staphylococcal Enterotoxin B
Rajagopalan G, Smart M, Patel R, David C. Acute Systemic Immune Activation following Conjunctival Exposure to Staphylococcal Enterotoxin B. Infection And Immunity 2006, 74: 6016-6019. PMID: 16988282, PMCID: PMC1594882, DOI: 10.1128/iai.00671-06.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesConjunctivaEnterotoxinsHistocompatibility Antigens Class IIHLA AntigensHumansLymphocyte ActivationMiceMice, TransgenicINTRANASAL EXPOSURE TO STAPHYLOCOCCAL ENTEROTOXIN B ELICITS AN ACUTE SYSTEMIC INFLAMMATORY RESPONSE
Rajagopalan G, Sen M, Singh M, Murali N, Nath K, Iijima K, Kita H, Leontovich A, Gopinathan U, Patel R, David C. INTRANASAL EXPOSURE TO STAPHYLOCOCCAL ENTEROTOXIN B ELICITS AN ACUTE SYSTEMIC INFLAMMATORY RESPONSE. Shock 2006, 25: 647-656. PMID: 16721274, DOI: 10.1097/01.shk.0000209565.92445.7d.Peer-Reviewed Original ResearchMeSH KeywordsAdministration, IntranasalAnimalsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCytokinesEnterotoxinsGene Expression RegulationHLA-DR3 AntigenHumansInflammationLungMiceMice, KnockoutNeutrophil InfiltrationReceptors, Interleukin-2Receptors, Interleukin-4Signal TransductionSystemic Inflammatory Response SyndromeConceptsII transgenic miceHLA class II transgenic miceStaphylococcal enterotoxin BCD8 T cellsTransgenic miceIntranasal exposureIL-12T cellsIFN-gammaEndogenous class II moleculesSystemic inflammatory response syndromeTCR V beta 8Defective IL-12Serum IFN-gammaSystemic immune activationInflammatory response syndromeSystemic cytokine responseBronchoalveolar lavage fluidMononuclear cell infiltrationPoor immune responsePro-inflammatory cytokinesS. aureus colonizationClass II moleculesIL-4 receptorNeutrophil influx
2002
Expression and Function of Transgenic HLA-DQ Molecules and Lymphocyte Development in Mice Lacking Invariant Chain
Rajagopalan G, Smart M, Krco C, David C. Expression and Function of Transgenic HLA-DQ Molecules and Lymphocyte Development in Mice Lacking Invariant Chain. The Journal Of Immunology 2002, 169: 1774-1783. PMID: 12165499, DOI: 10.4049/jimmunol.169.4.1774.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigen PresentationAntigensAntigens, Differentiation, B-LymphocyteB-LymphocytesCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell DifferentiationCytoskeletal ProteinsEnterotoxinsGene ExpressionHistocompatibility Antigens Class IIHLA-DQ AntigensHumansIn Vitro TechniquesInterferon-gammaLymphocyte ActivationLymphocyte SubsetsMiceMice, Inbred BALB CMice, Inbred C57BLMice, KnockoutMice, TransgenicShock, SepticConceptsClass II moleculesStaphylococcal enterotoxin BMHC class II moleculesT cellsFunctional MHC class II moleculesSystemic IFN-gamma productionT cell responsesHuman class II moleculesIFN-gamma productionPrimed T cellsHLA-DQ moleculesInvariant chainSpecific T cell hybridomasProcessing/presentationT cell hybridomasT cell developmentDQ8 miceExogenous superantigensHLA-DQ8Mature B cellsCytokine productionHLA-DQ6Phenotype of miceVivo challengeB cells