2022
Blood Transcriptomes of SARS-CoV-2–Infected Kidney Transplant Recipients Associated with Immune Insufficiency Proportionate to Severity
Sun Z, Zhang Z, Banu K, Al Azzi Y, Reghuvaran A, Fredericks S, Planoutene M, Hartzell S, Kim Y, Pell J, Tietjen G, Asch W, Kulkarni S, Formica R, Rana M, Maltzman JS, Zhang W, Akalin E, Heeger PS, Cravedi P, Menon MC. Blood Transcriptomes of SARS-CoV-2–Infected Kidney Transplant Recipients Associated with Immune Insufficiency Proportionate to Severity. Journal Of The American Society Of Nephrology 2022, 33: 2108-2122. PMID: 36041788, PMCID: PMC9678030, DOI: 10.1681/asn.2022010125.Peer-Reviewed Original ResearchConceptsKidney transplant recipientsImmune activation pathwaysImmunosuppressant useKTR cohortAcute illnessBlood transcriptomeAcute casesT cellsCOVID-19Most kidney transplant recipientsPost-acute COVID-19Adaptive immune system activationManagement of immunosuppressionReinstitution of immunosuppressionAcute COVID-19Serum inflammatory cytokinesCOVID-19 severity scoreCOVID-19 infectionImmune system activationUpregulation of neutrophilActivation pathwayTransplant recipientsChart reviewImmune signaturesLymphocyte count
2013
Alloantibody and Complement Promote T Cell–Mediated Cardiac Allograft Vasculopathy Through Noncanonical Nuclear Factor-&kgr;B Signaling in Endothelial Cells
Jane-wit D, Manes TD, Yi T, Qin L, Clark P, Kirkiles-Smith NC, Abrahimi P, Devalliere J, Moeckel G, Kulkarni S, Tellides G, Pober JS. Alloantibody and Complement Promote T Cell–Mediated Cardiac Allograft Vasculopathy Through Noncanonical Nuclear Factor-&kgr;B Signaling in Endothelial Cells. Circulation 2013, 128: 2504-2516. PMID: 24045046, PMCID: PMC3885874, DOI: 10.1161/circulationaha.113.002972.Peer-Reviewed Original ResearchConceptsCardiac allograft vasculopathyPanel reactive antibodyNuclear factor-κB signalingFactor-κB signalingAllograft vasculopathyT cellsEndothelial cellsMembrane attack complexAlloreactive T cell activationChronic antibody-mediated rejectionNoncanonical nuclear factorProinflammatory gene programAntibody-mediated rejectionDonor-specific antibodiesGraft endothelial cellsLate allograft lossAlloreactive T cellsAllogeneic endothelial cellsT cell activationAttack complexHuman T cellsAllograft lossHeart transplantationTransplantation patientsLesion pathogenesisRapamycin-treated human endothelial cells preferentially activate allogeneic regulatory T cells
Wang C, Yi T, Qin L, Maldonado RA, von Andrian UH, Kulkarni S, Tellides G, Pober JS. Rapamycin-treated human endothelial cells preferentially activate allogeneic regulatory T cells. Journal Of Clinical Investigation 2013, 123: 1677-1693. PMID: 23478407, PMCID: PMC3613923, DOI: 10.1172/jci66204.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsArteriesB7-H1 AntigenCD4-Positive T-LymphocytesCell ProliferationCells, CulturedCoculture TechniquesFemaleGene ExpressionGene Knockdown TechniquesHuman Umbilical Vein Endothelial CellsHumansImmunosuppression TherapyInterleukin-6Lymphocyte ActivationMiceMice, SCIDProgrammed Cell Death 1 Ligand 2 ProteinRegulatory-Associated Protein of mTORRNA, Small InterferingSirolimusT-Lymphocytes, RegulatoryTOR Serine-Threonine KinasesTranscriptional ActivationTransplantation, HomologousConceptsEffect of rapamycinT cellsEndothelial cellsAllograft rejectionHuman endothelial cellsPD-L1PD-L2Allogeneic regulatory T cellsHuman-mouse chimeric modelInhibitory molecule PD-L1Inflammatory cytokines IL-6Alloantigen-specific mannerAllograft endothelial cellsHuman arterial allograftsImmune-mediated rejectionGraft endothelial cellsEffector T cellsRegulatory T cellsMemory T cellsT cell responsesAntigen-presenting cellsCytokines IL-6Mock-treated cellsAllogeneic CD4Effector cytokines
2011
Neutralizing IL-6 Reduces Human Arterial Allograft Rejection by Allowing Emergence of CD161+ CD4+ Regulatory T Cells
Fogal B, Yi T, Wang C, Rao DA, Lebastchi A, Kulkarni S, Tellides G, Pober JS. Neutralizing IL-6 Reduces Human Arterial Allograft Rejection by Allowing Emergence of CD161+ CD4+ Regulatory T Cells. The Journal Of Immunology 2011, 187: 6268-6280. PMID: 22084439, PMCID: PMC3237826, DOI: 10.4049/jimmunol.1003774.Peer-Reviewed Original ResearchMeSH KeywordsAdultAnimalsCell DifferentiationCells, CulturedChemotaxis, LeukocyteCoculture TechniquesCoronary VesselsDisease Models, AnimalEndothelium, VascularFemaleGraft RejectionHuman Umbilical Vein Endothelial CellsHumansInterleukin-6MiceMice, SCIDMyocytes, Smooth MuscleNeutralization TestsNK Cell Lectin-Like Receptor Subfamily BT-Lymphocytes, RegulatoryConceptsRegulatory T cellsT cell infiltrationMemory T cellsT cell proliferationT cellsIL-6Allograft rejectionCell infiltrationIntimal expansionEffector memory T cellsHuman coronary artery segmentsEndothelial cellsEnhanced T cell proliferationHuman allograft rejectionT-cell infiltratesExpression of Foxp3Coronary artery segmentsCell proliferationMHC class IIIL-6 transcriptsT cell activationImmunodeficient mouse hostsHuman IL-6Allograft vesselsPerioperative injuryReperfusion Injury Intensifies the Adaptive Human T Cell Alloresponse in a Human-Mouse Chimeric Artery Model
Yi T, Fogal B, Hao Z, Tobiasova Z, Wang C, Rao DA, Al-Lamki RS, Kirkiles-Smith NC, Kulkarni S, Bradley JR, Bothwell AL, Sessa WC, Tellides G, Pober JS. Reperfusion Injury Intensifies the Adaptive Human T Cell Alloresponse in a Human-Mouse Chimeric Artery Model. Arteriosclerosis Thrombosis And Vascular Biology 2011, 32: 353-360. PMID: 22053072, PMCID: PMC3262100, DOI: 10.1161/atvbaha.111.239285.Peer-Reviewed Original ResearchConceptsArtery segmentsReperfusion injuryNonimmune injuryHuman artery segmentsHuman-mouse chimeric modelInfrarenal aortic interposition graftsT-cell-mediated injuryMouse hostHuman peripheral blood mononuclear cellsPeripheral blood mononuclear cellsCell-mediated injuryT cell alloresponseBlood mononuclear cellsAdaptive immune responsesAortic interposition graftsImmunodeficient mouse hostsGraft survivalInterposition graftImmunologic rejectionMononuclear cellsT cellsImmune responseMinimal sequelaeChimeric modelInjuryPeroxisome Proliferator–Activated Receptor-γ Agonists Prevent In Vivo Remodeling of Human Artery Induced by Alloreactive T Cells
Tobiasova Z, Zhang L, Yi T, Qin L, Manes TD, Kulkarni S, Lorber MI, Rodriguez FC, Choi JM, Tellides G, Pober JS, Kawikova I, Bothwell AL. Peroxisome Proliferator–Activated Receptor-γ Agonists Prevent In Vivo Remodeling of Human Artery Induced by Alloreactive T Cells. Circulation 2011, 124: 196-205. PMID: 21690493, PMCID: PMC3347886, DOI: 10.1161/circulationaha.110.015396.Peer-Reviewed Original ResearchMeSH KeywordsAdoptive TransferAnilidesAnimalsArteriesCell MovementCell ProliferationCytokinesGraft RejectionHumansHypoglycemic AgentsImmunologic MemoryIsoantigensMiceMice, SCIDPioglitazonePPAR gammaProstaglandin D2SuperantigensThiazolidinedionesT-LymphocytesTransplantation, HeterologousTransplantation, HomologousConceptsT cell responsesMemory T cellsVascular graft rejectionT cellsPPARγ agonistsVascular rejectionGraft rejectionAllogeneic human peripheral blood mononuclear cellsHuman memory T-cell responsesHuman T cell responsesMemory T cell responsesHuman peripheral blood mononuclear cellsTranscription factor peroxisome proliferator-activated receptorPeripheral blood mononuclear cellsChronic graft lossPeroxisome proliferator-activated receptorT-cell infiltratesAllogeneic T cellsAlloreactive T cellsBlood mononuclear cellsAlloantigen-induced proliferationVascular cell activationHuman arteriesProliferator-activated receptorEffects of PPARγ