2014
A TNFSF15 disease-risk polymorphism increases pattern-recognition receptor-induced signaling through caspase-8–induced IL-1
Hedl M, Abraham C. A TNFSF15 disease-risk polymorphism increases pattern-recognition receptor-induced signaling through caspase-8–induced IL-1. Proceedings Of The National Academy Of Sciences Of The United States Of America 2014, 111: 13451-13456. PMID: 25197060, PMCID: PMC4169936, DOI: 10.1073/pnas.1404178111.Peer-Reviewed Original ResearchMeSH KeywordsAcetylmuramyl-Alanyl-IsoglutamineADAM ProteinsADAM17 ProteinCaspase 8Cells, CulturedGenetic Predisposition to DiseaseHumansInterleukin-1LigandsMacrophagesMitogen-Activated Protein KinasesMycobacteriumMyeloid CellsNF-kappa BNod2 Signaling Adaptor ProteinPhosphatidylinositol 3-KinasesPolymorphism, Single NucleotideReceptors, Pattern RecognitionReceptors, Tumor Necrosis Factor, Member 25Signal TransductionSolubilityTissue Inhibitor of Metalloproteinase-3Tumor Necrosis Factor Ligand Superfamily Member 15ConceptsMost risk lociCaspase-8-dependent pathwayCytokine secretionGain of functionIntestinal myeloid cellsInflammatory bowel diseaseRisk lociIL-1 secretionTNFSF15 expressionPI3KPRR responsesBowel diseaseSignalingCytokine productionImmune homeostasisInflammatory diseasesHuman macrophagesIL-1Myeloid cellsAltered functionCytokinesTNFSF15MacrophagesSecretionDisease
1991
Interleukin-1 corrects the defective autologous mixed lymphocyte response in multiple sclerosis
Hafler D, Chofflon M, Kurt-Jones E, Weiner H. Interleukin-1 corrects the defective autologous mixed lymphocyte response in multiple sclerosis. Clinical Immunology 1991, 58: 115-125. PMID: 1670583, DOI: 10.1016/0090-1229(91)90153-2.Peer-Reviewed Original ResearchConceptsAutologous mixed lymphocyte reactionMultiple sclerosisWhole T cellsMS patientsT cellsImmune defectsChronic progressive multiple sclerosisNon-T cell populationsAutologous mixed lymphocyte responseProgressive multiple sclerosisMixed lymphocyte responseMixed lymphocyte reactionResponse of CD4T cell populationsSex-matched controlsT cell regulationIL-1 secretionCell populationsLymphokine IFN-gammaImmunoregulatory defectsLymphocyte responsesRIL-2Lymphocyte reactionMS subjectsAutoimmune diseases
1989
ENDOTHELIAL CELL ACTIVATION AND HIGH INTERLEUKIN-1 SECRETION IN THE PATHOGENESIS OF ACUTE KAWASAKI DISEASE
Leung D, Kurt-Jones E, Newburger J, Cotran R, Burns J, Pober J. ENDOTHELIAL CELL ACTIVATION AND HIGH INTERLEUKIN-1 SECRETION IN THE PATHOGENESIS OF ACUTE KAWASAKI DISEASE. The Lancet 1989, 334: 1298-1302. PMID: 2480498, DOI: 10.1016/s0140-6736(89)91910-7.Peer-Reviewed Original ResearchMeSH KeywordsAntigens, SurfaceCell AdhesionCell Adhesion MoleculesChild, PreschoolE-SelectinEndothelium, VascularFemalegamma-GlobulinsHLA-DQ AntigensHumansImmunization, PassiveIntercellular Adhesion Molecule-1Interleukin-1MaleMembrane GlycoproteinsMucocutaneous Lymph Node SyndromeReceptors, ImmunologicSkinConceptsEndothelial cell activationCoronary artery abnormalitiesCell activationInterleukin-1Gammaglobulin treatmentArtery abnormalitiesKawasaki diseaseAcute Kawasaki disease patientsPeripheral blood mononuclear cellsEndothelial cellsCytotoxic antibody activityIntravenous gammaglobulin treatmentKawasaki disease patientsAcute Kawasaki diseaseEndothelial cell antigensBlood mononuclear cellsInterleukin-1 secretionTumor necrosis factorIL-1 secretionEndothelial cell expressionSkin biopsy samplesMeans of immunoperoxidaseMucocutaneous symptomsPersistent feverClinical symptoms
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