2019
PD-1H (VISTA)–mediated suppression of autoimmunity in systemic and cutaneous lupus erythematosus
Han X, Vesely MD, Yang W, Sanmamed MF, Badri T, Alawa J, López-Giráldez F, Gaule P, Lee SW, Zhang JP, Nie X, Nassar A, Boto A, Flies DB, Zheng L, Kim TK, Moeckel GW, McNiff JM, Chen L. PD-1H (VISTA)–mediated suppression of autoimmunity in systemic and cutaneous lupus erythematosus. Science Translational Medicine 2019, 11 PMID: 31826980, DOI: 10.1126/scitranslmed.aax1159.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsArthritisAutoantibodiesAutoimmunityDendritic CellsHumansInflammationInterferon Type ILupus Erythematosus, CutaneousLupus Erythematosus, SystemicMembrane ProteinsMice, Inbred BALB CMice, Inbred MRL lprMyeloid CellsNeutrophilsReceptors, Antigen, T-CellSignal TransductionTerpenesUp-RegulationConceptsPlasmacytoid dendritic cellsDiscoid lupus erythematosusSystemic lupus erythematosusCutaneous lupus lesionsPD-1HLupus erythematosusLupus lesionsAutoimmune diseasesKO miceT cellsMyeloid cellsHuman systemic lupus erythematosusBALB/c backgroundCutaneous lupus erythematosusInappropriate immune responseProgression of lupusSystemic autoimmune diseaseImmune cell expansionSuppression of autoimmunityAgonistic monoclonal antibodyDeath-1 homologCutaneous lupusProinflammatory neutrophilsDendritic cellsDLE lesions
2014
Chemokine receptor Cxcr4 contributes to kidney fibrosis via multiple effectors
Yuan A, Lee Y, Choi U, Moeckel G, Karihaloo A. Chemokine receptor Cxcr4 contributes to kidney fibrosis via multiple effectors. American Journal Of Physiology. Renal Physiology 2014, 308: f459-f472. PMID: 25537742, PMCID: PMC4346747, DOI: 10.1152/ajprenal.00146.2014.Peer-Reviewed Original ResearchConceptsUnilateral ureteral obstructionCXCR4 expressionKidney fibrosisChemokine receptorsFibrotic responseSmooth muscle actin levelsG protein-coupled chemokine receptorsGrowth factorChronic kidney inflammationProgressive tissue injuryChronic kidney diseaseHigh CXCR4 expressionTGF-β1 levelsEffector cell typesProgression of fibrosisScarring/fibrosisFinal common pathwayPlatelet-derived growth factorRenal injuryKidney inflammationObstructed kidneysBone morphogenetic protein-7Renal fibrosisUreteral obstructionKidney diseaseGM-CSF Promotes Macrophage Alternative Activation after Renal Ischemia/Reperfusion Injury
Huen SC, Huynh L, Marlier A, Lee Y, Moeckel GW, Cantley LG. GM-CSF Promotes Macrophage Alternative Activation after Renal Ischemia/Reperfusion Injury. Journal Of The American Society Of Nephrology 2014, 26: 1334-1345. PMID: 25388222, PMCID: PMC4446881, DOI: 10.1681/asn.2014060612.Peer-Reviewed Original ResearchMeSH KeywordsAcute Kidney InjuryAnalysis of VarianceAnimalsBlotting, WesternCell ProliferationCells, CulturedDisease Models, AnimalGene Expression RegulationGranulocyte-Macrophage Colony-Stimulating FactorImmunohistochemistryKidney Tubules, ProximalMacrophage ActivationMaleMiceMice, Inbred C57BLMultivariate AnalysisPhenotypeRandom AllocationReal-Time Polymerase Chain ReactionReperfusion InjurySignal TransductionUp-RegulationConceptsIschemia/reperfusion injuryMacrophage alternative activationBone marrow-derived macrophagesAlternative activationMarrow-derived macrophagesTubular cellsGM-CSFReperfusion injuryReparative phenotypeTubular proliferationKidney ischemia/reperfusion injuryRenal ischemia/reperfusion injuryMouse proximal tubule cellsInitial kidney damageRepair phaseProximal tubule cellsTubular factorsIschemic injuryKidney damageProinflammatory macrophagesRenal repairMacrophage activationTubule cellsPharmacologic inhibitionMacrophages