2025
Immune dysregulation in glycogen storage disease 1b extends beyond neutropenia
Gehlhaar A, Shouval D, Santiago E, Ling G, McCourt B, Werner L, Yerushalmi B, Konnikova L. Immune dysregulation in glycogen storage disease 1b extends beyond neutropenia. Human Immunology 2025, 86: 111268. PMID: 40037121, DOI: 10.1016/j.humimm.2025.111268.Peer-Reviewed Original ResearchGlycogen storage disease type 1bGlycogen storage disease type 1b patientsImpaired immune cell traffickingClassic treatment strategiesUpregulation of CXCR3Effector memory phenotypeT cell populationsNatural killer cellsSystems immunology approachNon-classical monocytesImmune cell traffickingGlycogen storage disease 1bImmune defectsMemory phenotypeMultiple T cell populationsImmune landscapeRecurrent infectionsKiller cellsImmune dysregulationImmune impairmentImmunophenotypic characterizationSLC37A4 geneControl subjectsTreatment strategiesNeutrophil numbers
2022
Immune-mediated tubule atrophy promotes acute kidney injury to chronic kidney disease transition
Xu L, Guo J, Moledina DG, Cantley LG. Immune-mediated tubule atrophy promotes acute kidney injury to chronic kidney disease transition. Nature Communications 2022, 13: 4892. PMID: 35986026, PMCID: PMC9391331, DOI: 10.1038/s41467-022-32634-0.Peer-Reviewed Original ResearchConceptsAcute kidney injuryKidney injuryT cellsChronic kidney disease transitionIschemia-reperfusion kidney injuryKidney disease transitionChronic kidney diseaseDepletion of neutrophilsGlomerular filtration rateT cell recruitmentTubular cell lossMacrophage persistenceProinflammatory neutrophilsTubule damageKidney atrophyContralateral kidneyNeutrophil numbersContralateral nephrectomyKidney diseaseTubule atrophyFiltration rateCell recruitmentMore macrophagesDay 14Day 5
2020
Abnormal Neutrophil Transcriptional Signature May Predict Newly Diagnosed Latent Autoimmune Diabetes in Adults of South China
Xing Y, Lin Q, Tong Y, Zhou W, Huang J, Wang Y, Huang G, Li Y, Xiang Z, Zhou Z, Li T, Xiao Y. Abnormal Neutrophil Transcriptional Signature May Predict Newly Diagnosed Latent Autoimmune Diabetes in Adults of South China. Frontiers In Endocrinology 2020, 11: 581902. PMID: 33391182, PMCID: PMC7775642, DOI: 10.3389/fendo.2020.581902.Peer-Reviewed Original ResearchConceptsSex-matched healthy controlsLADA patientsHealthy controlsDevelopment of LADAPathological processesPeripheral blood neutrophilsCytokine-cytokine receptor interactionReal-time polymerase chain reactionLatent AutoimmuneAdhesion molecule signalingAutoimmune diabetesFunction deteriorationNeutrophil numbersPeripheral neutrophilsBlood neutrophilsPolymerase chain reactionPathological alterationsCell differentiationLeukocyte degranulationMyeloid cell differentiationGenomes (KEGG) pathway enrichmentPatientsPresent study resultsNeutrophilsTranscriptional level
2018
Distinct neutrophil counts and functions in newly diagnosed type 1 diabetes, latent autoimmune diabetes in adults, and type 2 diabetes
Huang J, Xiao Y, Zheng P, Zhou W, Wang Y, Huang G, Xu A, Zhou Z. Distinct neutrophil counts and functions in newly diagnosed type 1 diabetes, latent autoimmune diabetes in adults, and type 2 diabetes. Diabetes/Metabolism Research And Reviews 2018, 35: e3064. PMID: 30123986, DOI: 10.1002/dmrr.3064.Peer-Reviewed Original ResearchConceptsNeutrophil countType 1 diabetesT1D patientsNeutrophil numbersPhagocytosis rateTitres of autoantibodiesΒ-cell antigensΒ-cell autoimmunityChemokine receptor expressionType 2 diabetesMigration of neutrophilsLADA patientsPositive autoantibodiesAutoimmune diabetesChemokine levelsCD62L expressionT2D patientsClinical parametersNeutrophil migrationHealthy controlsReceptor expressionAnimal modelsDiabetesPatientsDifferent subtypes
2014
SRF is required for neutrophil migration in response to inflammation
Taylor A, Tang W, Bruscia EM, Zhang PX, Lin A, Gaines P, Wu D, Halene S. SRF is required for neutrophil migration in response to inflammation. Blood 2014, 123: 3027-3036. PMID: 24574460, PMCID: PMC4014845, DOI: 10.1182/blood-2013-06-507582.Peer-Reviewed Original ResearchMeSH KeywordsActin CytoskeletonActinsAnimalsBlotting, WesternCell AdhesionCell MovementChemokinesGene ExpressionInflammationIntegrinsMiceMice, KnockoutMice, TransgenicMicroscopy, ConfocalN-Formylmethionine Leucyl-PhenylalanineNeutrophilsPolymerizationReverse Transcriptase Polymerase Chain ReactionSerum Response FactorSignal TransductionConceptsKO neutrophilsNeutrophil functionNormal neutrophil numbersSerum response factorSites of inflammationRole of SRFLoss of SRFNeutrophil numbersNeutrophil migrationMalignant processNeutrophilsCytokine stimuliChemokine gradientsCell functionExpression levelsIntegrin expression levelsInflammationMicePrimary defenseMegakaryocyte maturationNormal cell functionVivoCellular adhesionMaster regulatorIntegrin activation
2007
IL-12/23p40-dependent clearance of Anaplasma phagocytophilum in the murine model of human anaplasmosis
Pedra JH, Tao J, Sutterwala FS, Sukumaran B, Berliner N, Bockenstedt LK, Flavell RA, Yin Z, Fikrig E. IL-12/23p40-dependent clearance of Anaplasma phagocytophilum in the murine model of human anaplasmosis. Pathogens And Disease 2007, 50: 401-410. PMID: 17521390, DOI: 10.1111/j.1574-695x.2007.00270.x.Peer-Reviewed Original ResearchConceptsIL-12/23p40Deficient miceT cellsImmune responseHuman anaplasmosisTh1 immune responseIFN-gamma productionDay 6 postinfectionAnaplasma phagocytophilumA. phagocytophilum burdenIL-23Dendritic cellsIL-12Neutrophil numbersIFN-gammaMurine modelMicrobial agonistsPathogen clearanceDependent clearanceInfectious diseasesEarly susceptibilityPathogen eliminationCausative agentA. phagocytophilumIndependent mechanisms
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