2018
SIRT6 Acts as a Negative Regulator in Dengue Virus-Induced Inflammatory Response by Targeting the DNA Binding Domain of NF-κB p65
Li P, Jin Y, Qi F, Wu F, Luo S, Cheng Y, Montgomery RR, Qian F. SIRT6 Acts as a Negative Regulator in Dengue Virus-Induced Inflammatory Response by Targeting the DNA Binding Domain of NF-κB p65. Frontiers In Cellular And Infection Microbiology 2018, 8: 113. PMID: 29686974, PMCID: PMC5900784, DOI: 10.3389/fcimb.2018.00113.Peer-Reviewed Original ResearchConceptsToll-like receptor 3Dengue virusInflammatory responseDENV infectionDengue disease severityNF-κB p65Innate immune responseNF-κB activationDomain of p65Overexpression of SIRT6Chemokine productionProinflammatory cytokinesDengue patientsInflammatory cytokinesP65 functionImmune responseLike receptorsDisease severityNegative regulatorReceptor 3Variable severityP65SIRT6CytokinesVirus
2017
Aging impairs both primary and secondary RIG-I signaling for interferon induction in human monocytes
Molony RD, Nguyen JT, Kong Y, Montgomery RR, Shaw AC, Iwasaki A. Aging impairs both primary and secondary RIG-I signaling for interferon induction in human monocytes. Science Signaling 2017, 10 PMID: 29233916, PMCID: PMC6429941, DOI: 10.1126/scisignal.aan2392.Peer-Reviewed Original ResearchMeSH KeywordsAdultAgedAged, 80 and overAgingDEAD Box Protein 58FemaleHumansImmunity, InnateInterferonsMaleMonocytesReceptors, ImmunologicSignal TransductionConceptsType I IFNsI IFNsI interferonOlder adultsIFN inductionRetinoic acid-inducible gene IAcid-inducible gene IHealthy human donorsType I interferonRespiratory influenzaProinflammatory cytokinesVirus infectionType I IFN genesAdult monocytesAntiviral resistanceTranscription factor IRF8IFN responseHuman donorsMonocytesIncreased proteasomal degradationHuman monocytesYoung adultsIRF8 expressionIAV RNAInfected cellsHumanized mouse model supports development, function, and tissue residency of human natural killer cells
Herndler-Brandstetter D, Shan L, Yao Y, Stecher C, Plajer V, Lietzenmayer M, Strowig T, de Zoete MR, Palm NW, Chen J, Blish CA, Frleta D, Gurer C, Macdonald LE, Murphy AJ, Yancopoulos GD, Montgomery RR, Flavell RA. Humanized mouse model supports development, function, and tissue residency of human natural killer cells. Proceedings Of The National Academy Of Sciences Of The United States Of America 2017, 114: e9626-e9634. PMID: 29078283, PMCID: PMC5692533, DOI: 10.1073/pnas.1705301114.Peer-Reviewed Original ResearchConceptsHuman natural killer cellsNatural killer cellsHumanized mouse modelCell subsetsKiller cellsLymphoma xenograftsHuman NKMouse modelHuman antitumor immune responsesHuman NK cell subsetsInnate lymphoid cell subsetsBurkitt's lymphoma xenograftsNK cell subpopulationsNK cell subsetsAntitumor immune responseT cell subsetsHuman NK cellsKiller inhibitory receptorsLymphoid cell subsetsSignal regulatory protein alphaHuman immune systemHuman interleukin-15Regulatory protein alphaNK cellsHumanized mice
2014
Effect of aging on microRNAs and regulation of pathogen recognition receptors
Olivieri F, Procopio AD, Montgomery RR. Effect of aging on microRNAs and regulation of pathogen recognition receptors. Current Opinion In Immunology 2014, 29: 29-37. PMID: 24769423, PMCID: PMC4119513, DOI: 10.1016/j.coi.2014.03.006.Peer-Reviewed Original ResearchMeSH KeywordsAdaptive ImmunityAgingAnimalsHumansImmunity, InnateInflammationMicroRNAsReceptors, ImmunologicConceptsInnate immune recognitionImmune innate responseResolution of inflammationPathogen recognition receptorsTLR signalsUnderstanding of immunosenescenceProinflammatory responseImmune responseNF-κBInnate responseImmune recognitionRecognition receptorsActive investigationImmunosenescenceDownstream effectorsRecent studiesNegative regulatorSimilar regulatory activitiesResponseMiRNAsInflammationMicroRNAsAging-associated miRNAsVaccine
2004
Myeloid Differentiation Antigen 88 Deficiency Impairs Pathogen Clearance but Does Not Alter Inflammation in Borrelia burgdorferi-Infected Mice
Liu N, Montgomery RR, Barthold SW, Bockenstedt LK. Myeloid Differentiation Antigen 88 Deficiency Impairs Pathogen Clearance but Does Not Alter Inflammation in Borrelia burgdorferi-Infected Mice. Infection And Immunity 2004, 72: 3195-3203. PMID: 15155621, PMCID: PMC415708, DOI: 10.1128/iai.72.6.3195-3203.2004.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingAnimalsAntibodies, BacterialAntigens, DifferentiationArthritisBorrelia burgdorferiDNA, BacterialInflammationLyme DiseaseMacrophages, PeritonealMiceMice, Inbred C57BLMice, KnockoutMyeloid Differentiation Factor 88MyocarditisOpsonin ProteinsPhagocytosisReceptors, ImmunologicUrineConceptsToll-like receptor 2Days of infectionPathogen burdenWT miceAcute inflammationB. burgdorferi-specific antibodyPathogen-specific adaptive immunityMyD88-dependent signaling pathwaysTumor necrosis factor alphaBurgdorferi-specific antibodiesImmunoglobulin G1 responsesTLR2-deficient miceInnate immune cellsBorrelia burgdorferiNecrosis factor alphaWild-type miceIgM titersImmune cellsInflammatory responseFactor alphaAdaptive immunitySpirochete Borrelia burgdorferiWT macrophagesReceptor 2Pathogen clearance