2023
HSV-2 triggers upregulation of MALAT1 in CD4+ T cells and promotes HIV latency reversal
Pierce C, Loh L, Steach H, Cheshenko N, Preston-Hurlburt P, Zhang F, Stransky S, Kravets L, Sidoli S, Philbrick W, Nassar M, Krishnaswamy S, Herold K, Herold B. HSV-2 triggers upregulation of MALAT1 in CD4+ T cells and promotes HIV latency reversal. Journal Of Clinical Investigation 2023, 133: e164317. PMID: 37079384, PMCID: PMC10232005, DOI: 10.1172/jci164317.Peer-Reviewed Original ResearchConceptsHIV-1 reactivationHIV latency reversalT cellsLatency reversalHuman CD4HIV-1 viral loadHIV-1 restriction factorsHSV-2 recurrencesHSV-2 infectionHIV-1 latencyUpregulation of MALAT1Primary human CD4HSV-2 proteinsViral loadHIV replicationPeripheral bloodMALAT1 expressionHSV-2Tissue reservoirsCD4Viral replicationExpression of transcriptsBystander cellsRestriction factorsMALAT1
2016
The Receptor for Advanced Glycation Endproducts Drives T Cell Survival and Inflammation in Type 1 Diabetes Mellitus
Durning SP, Preston-Hurlburt P, Clark PR, Xu D, Herold KC, Group T. The Receptor for Advanced Glycation Endproducts Drives T Cell Survival and Inflammation in Type 1 Diabetes Mellitus. The Journal Of Immunology 2016, 197: 3076-3085. PMID: 27655844, PMCID: PMC5101164, DOI: 10.4049/jimmunol.1600197.Peer-Reviewed Original ResearchMeSH KeywordsAdolescentAdultAsymptomatic DiseasesCD8-Positive T-LymphocytesCell SurvivalCells, CulturedChildDiabetes Mellitus, Type 1Disease ProgressionFemaleGene Expression ProfilingHumansImmunologic MemoryInflammationLymphocyte ActivationMaleReceptor for Advanced Glycation End ProductsRiskSignal TransductionUp-RegulationYoung AdultConceptsDamage-associated molecular patternsT cellsRAGE expressionT1D patientsInflammatory functionsRisk relativesCell activationHigh mobility group box 1Mobility group box 1Advanced glycated endproductsChronic autoimmune responseMolecular patternsEffector memory cellsHealthy control subjectsExpression of RAGEGroup box 1Type 1 diabetesAdvanced glycation endproductsT cell survivalAutoimmune responseAutoimmune diseasesControl subjectsDisease onsetRisk subjectsCell injury