2019
LACC1 Required for NOD2-Induced, ER Stress-Mediated Innate Immune Outcomes in Human Macrophages and LACC1 Risk Variants Modulate These Outcomes
Huang C, Hedl M, Ranjan K, Abraham C. LACC1 Required for NOD2-Induced, ER Stress-Mediated Innate Immune Outcomes in Human Macrophages and LACC1 Risk Variants Modulate These Outcomes. Cell Reports 2019, 29: 4525-4539.e4. PMID: 31875558, PMCID: PMC7372507, DOI: 10.1016/j.celrep.2019.11.105.Peer-Reviewed Original ResearchMeSH KeywordsActivating Transcription Factor 6EIF-2 KinaseEndoplasmic ReticulumEndoplasmic Reticulum StressEndoribonucleasesEnterococcus faecalisEscherichia coliGene Expression RegulationHeLa CellsHost-Pathogen InteractionsHumansImmunity, InnateIntracellular Signaling Peptides and ProteinsMacrophagesNod2 Signaling Adaptor ProteinPhagocytosisPrimary Cell CultureProtein Serine-Threonine KinasesRiskSignal TransductionConceptsEndoplasmic reticulumER stressER stress sensorsHuman macrophagesInnate immune outcomesDisease risk variantsMultiple immune-mediated diseasesLaccase domainPattern recognition receptor NOD2HeLa cellsAntimicrobial pathwaysRisk variantsGenetic variantsLACC1Critical roleVariantsMacrophagesATF6IRE1αArg284SignalingReticulumStressTransfectionPERK
2011
Inflammatory disease protective R381Q IL23 receptor polymorphism results in decreased primary CD4+ and CD8+ human T-cell functional responses
Sarin R, Wu X, Abraham C. Inflammatory disease protective R381Q IL23 receptor polymorphism results in decreased primary CD4+ and CD8+ human T-cell functional responses. Proceedings Of The National Academy Of Sciences Of The United States Of America 2011, 108: 9560-9565. PMID: 21606346, PMCID: PMC3111257, DOI: 10.1073/pnas.1017854108.Peer-Reviewed Original ResearchMeSH KeywordsCD4-Positive T-LymphocytesCD8-Positive T-LymphocytesCell ProliferationCells, CulturedFlow CytometryHEK293 CellsHeLa CellsHumansImmunoblottingInflammatory Bowel DiseasesInterferon-gammaInterleukin-17Interleukin-23InterleukinsLuciferasesPolymorphism, Single NucleotideReceptors, InterleukinSignal TransductionSTAT3 Transcription FactorTh17 CellsConceptsT cellsIL-22 productionIL-23 receptorT cell functional responsesMultiple inflammatory diseasesPrimary human CD4WT CD8Tc17 cellsIL-17Arginine alleleInflammatory diseasesReceptor polymorphismsPrimary CD4Transcription 3 (STAT3) activationCD8Human CD4Function alterationsSignificant protectionHuman genetic polymorphismsGenetic polymorphismsR381QCD4AutoimmunityFunctional consequencesSignal transducer