2023
Enhanced inhibition of MHC-I expression by SARS-CoV-2 Omicron subvariants
Moriyama M, Lucas C, Monteiro V, Initiative Y, Iwasaki A, Chen N, Breban M, Hahn A, Pham K, Koch T, Chaguza C, Tikhonova I, Castaldi C, Mane S, De Kumar B, Ferguson D, Kerantzas N, Peaper D, Landry M, Schulz W, Vogels C, Grubaugh N. Enhanced inhibition of MHC-I expression by SARS-CoV-2 Omicron subvariants. Proceedings Of The National Academy Of Sciences Of The United States Of America 2023, 120: e2221652120. PMID: 37036977, PMCID: PMC10120007, DOI: 10.1073/pnas.2221652120.Peer-Reviewed Original ResearchConceptsMHC-I expressionBreakthrough infectionsSevere acute respiratory syndrome coronavirus 2 (SARS-CoV-2) variantsMajor histocompatibility complex class I expressionCell-mediated immunityInfluenza virus infectionSARS-CoV-2 VOCsMHC-I upregulationClass I expressionSARS-CoV-2T cell recognitionVirus infectionMHC II expressionSpike proteinEnhanced inhibitionInfectionCell recognitionCommon mutationsReinfectionE proteinAntibodiesViral genesSubvariantsExpression
2022
SARS-CoV-2 accessory proteins ORF7a and ORF3a use distinct mechanisms to down-regulate MHC-I surface expression
Arshad N, Laurent-Rolle M, Ahmed W, Hsu J, Mitchell S, Pawlak J, Sengupta D, Biswas K, Cresswell P. SARS-CoV-2 accessory proteins ORF7a and ORF3a use distinct mechanisms to down-regulate MHC-I surface expression. Proceedings Of The National Academy Of Sciences Of The United States Of America 2022, 120: e2208525120. PMID: 36574644, PMCID: PMC9910621, DOI: 10.1073/pnas.2208525120.Peer-Reviewed Original ResearchConceptsMHC-I expressionSARS-CoV-2Major histocompatibility complex (MHC) class I moleculesT cell recognitionVirus-infected cellsClass I moleculesAntigen presentationOngoing COVID-19 pandemicHeavy chainImmune evasionViral peptidesSecretory pathwayDistinct mechanismsMHCI moleculesPeptide-MHCInfected cellsCausative agentCell recognitionCD8COVID-19 pandemicViral proteinsEndoplasmic reticulumHuman MHCORF7a
2021
Signal strength controls the rate of polarization within CTLs during killing
Frazer G, Gawden-Bone C, Dieckmann N, Asano Y, Griffiths G. Signal strength controls the rate of polarization within CTLs during killing. Journal Of Cell Biology 2021, 220: e202104093. PMID: 34292303, PMCID: PMC8302442, DOI: 10.1083/jcb.202104093.Peer-Reviewed Original ResearchConceptsCytotoxic T lymphocytesProportion of cytotoxic T lymphocytesTarget cellsEffector CTL responsesTCR signal strengthTarget cell recognitionCTL responsesDegree of killingEffector cellsT lymphocytesCytolytic granulesGranule polarizationImmune responseImmune synapseProlonged dwell timeKill targetsAmino acid changesCell recognitionGranule deliveryAcid changesSingle amino acid changesKillingCellsIncreasing proportionStrength of signal
2018
Loss of ADAR1 in tumours overcomes resistance to immune checkpoint blockade
Ishizuka JJ, Manguso RT, Cheruiyot CK, Bi K, Panda A, Iracheta-Vellve A, Miller BC, Du PP, Yates KB, Dubrot J, Buchumenski I, Comstock DE, Brown FD, Ayer A, Kohnle IC, Pope HW, Zimmer MD, Sen DR, Lane-Reticker SK, Robitschek EJ, Griffin GK, Collins NB, Long AH, Doench JG, Kozono D, Levanon EY, Haining WN. Loss of ADAR1 in tumours overcomes resistance to immune checkpoint blockade. Nature 2018, 565: 43-48. PMID: 30559380, PMCID: PMC7241251, DOI: 10.1038/s41586-018-0768-9.Peer-Reviewed Original ResearchMeSH KeywordsAdenosine DeaminaseAnimalsCell Cycle CheckpointsCell Line, TumorCRISPR-Cas SystemsDrug Resistance, NeoplasmFemaleHistocompatibility Antigens Class IImmunotherapyInflammationInterferon-Induced Helicase, IFIH1InterferonsMelanoma, ExperimentalMiceMice, Inbred C57BLPhenotypeProgrammed Cell Death 1 ReceptorReceptors, G-Protein-CoupledRNA EditingRNA-Binding ProteinsRNA, Double-StrandedConceptsImmune checkpoint blockadeCheckpoint blockadeAntigen presentationEffective anti-tumor immunityPD-1 checkpoint blockadeTumor cellsAnti-tumor immunityT cell recognitionSufficient inflammationImmunotherapy resistanceInhibitory checkpointsMost patientsInnate ligandsLoss of functionBlockadeTherapeutic requirementsLoss of ADAR1TumorsCancer cellsCell recognitionInflammationGrowth inhibitionADAR1PresentationCells
2008
Cutting Edge: Engagement of NKG2A on CD8+ Effector T Cells Limits Immunopathology in Influenza Pneumonia
Zhou J, Matsuoka M, Cantor H, Homer R, Enelow RI. Cutting Edge: Engagement of NKG2A on CD8+ Effector T Cells Limits Immunopathology in Influenza Pneumonia. The Journal Of Immunology 2008, 180: 25-29. PMID: 18096998, DOI: 10.4049/jimmunol.180.1.25.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigensCD8-Positive T-LymphocytesHistocompatibility Antigens Class IInfluenza A virusMiceMice, Inbred BALB CMice, Inbred C57BLNK Cell Lectin-Like Receptor Subfamily CNK Cell Lectin-Like Receptor Subfamily DOrthomyxoviridae InfectionsPneumonia, ViralReceptors, ImmunologicReceptors, Natural Killer CellConceptsInfluenza pneumoniaT cellsLung injuryTNF productionT cell-mediated clearanceQa-1bAg-specific CD8Considerable lung injurySevere influenza infectionCD94/NKG2AT cell Ag recognitionEffector cell recognitionLimit immunopathologyNKG2A blockadeAntiviral CD8Distal airwaysInfluenza infectionPulmonary pathologyTNF-alphaCD8Infectious virusAg recognitionImmunopathologyPneumoniaCell recognition
2006
Mapping the Binding Site on CD8β for MHC Class I Reveals Mutants with Enhanced Binding
Devine L, Thakral D, Nag S, Dobbins J, Hodsdon ME, Kavathas PB. Mapping the Binding Site on CD8β for MHC Class I Reveals Mutants with Enhanced Binding. The Journal Of Immunology 2006, 177: 3930-3938. PMID: 16951356, DOI: 10.4049/jimmunol.177.6.3930.Peer-Reviewed Original ResearchConceptsMHC class IClass IT cellsT cell responsesEffective immune responseT cell recognitionT cell hybridomasT cell membraneImmune responseCoreceptor functionCell responsesCell hybridomasInfected cellsCell recognitionIdentified mutationsCD8alphaCoreceptorCD8betaCDR3 loopsCellsEnhanced bindingCD8ImmunotherapyCD8alphabetaCD8β
2002
Porcine Endothelial Cells, Unlike Human Endothelial Cells, Can Be Killed by Human CTL Via Fas Ligand and Cannot Be Protected by Bcl-2
Zheng L, Ben LH, Pober JS, Bothwell AL. Porcine Endothelial Cells, Unlike Human Endothelial Cells, Can Be Killed by Human CTL Via Fas Ligand and Cannot Be Protected by Bcl-2. The Journal Of Immunology 2002, 169: 6850-6855. PMID: 12471117, DOI: 10.4049/jimmunol.169.12.6850.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, HeterophileApoptosisCD8-Positive T-LymphocytesCell LineCell Line, TransformedCoculture TechniquesCytotoxicity Tests, ImmunologicCytotoxicity, ImmunologicEndothelium, VascularEpitopes, T-LymphocyteFas Ligand Proteinfas ReceptorGenetic VectorsGranzymesHistocompatibility Antigens Class IHumansImmunity, InnateIsoantigensLigandsMembrane GlycoproteinsPerforinPore Forming Cytotoxic ProteinsProto-Oncogene Proteins c-bcl-2Serine EndopeptidasesSwineT-Lymphocytes, CytotoxicConceptsHuman endothelial cellsPorcine endothelial cellsEndothelial cellsBcl-2MHC class I restrictionClass I restrictionPorcine aortic endothelial cellsTarget cell recognitionAnti-Fas ligand AbAortic endothelial cellsHost CTLAcute rejectionCTL responsesDrug-induced apoptosisHuman CTLPorcine targetsTarget cell typeHuman xenotransplantationFAS expressionFas ligandPorcine cellsCTLMajor effectorCell recognitionMajor target
1991
The Potential of Restricted T Cell Recognition of Myelin Basic Protein Epitopes in the Therapy of Multiple Sclerosis
HAFLER D, MATSUI M, WUCHERPFENNIG K, OTA K, WEINER H. The Potential of Restricted T Cell Recognition of Myelin Basic Protein Epitopes in the Therapy of Multiple Sclerosis. Annals Of The New York Academy Of Sciences 1991, 636: 251-265. PMID: 1724362, DOI: 10.1111/j.1749-6632.1991.tb33456.x.Peer-Reviewed Original ResearchConceptsMyelin basic protein epitopeT cell recognitionMultiple sclerosisCell recognitionProtein epitopesSclerosisTherapy
1981
The immune response to human type III and type V (AB2) collagen: antigenic determinants and genetic control in mice
Kemp J, Madri J. The immune response to human type III and type V (AB2) collagen: antigenic determinants and genetic control in mice. European Journal Of Immunology 1981, 11: 90-94. PMID: 6163643, DOI: 10.1002/eji.1830110205.Peer-Reviewed Original ResearchConceptsAntibody responseSpecific IgG antibody responseAntigenic determinantsIgG antibody responseHigher antibody responseT cell recognitionType IIIType IHuman type IIIHigh-affinity monoclonal antibodiesAntigen presentationImmune responseBovine collagen type IMonoclonal antibodiesCollagen type IIr genesType V collagenCell recognitionHuman collagenFurther studiesConnective tissue biologyTissue biologyMicePresent studyCollagen
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