2020
Complement activated interferon-γ-primed human endothelium transpresents interleukin-15 to CD8+ T cells
Xie CB, Jiang B, Qin L, Tellides G, Kirkiles-Smith NC, Jane-wit D, Pober JS. Complement activated interferon-γ-primed human endothelium transpresents interleukin-15 to CD8+ T cells. Journal Of Clinical Investigation 2020, 130: 3437-3452. PMID: 32191642, PMCID: PMC7324183, DOI: 10.1172/jci135060.Peer-Reviewed Original ResearchConceptsIL-15/IL-15Rα complexesIL-1βHuman endothelial cellsMembrane attack complexEndothelial cellsAcute rejectionT cellsT cell-mediated acute rejectionCell-mediated acute rejectionComplement-mediated pathologiesIL-15Rα expressionGraft endothelial cellsHuman coronary artery graftsEffector memory CD4T cell infiltrationCoronary artery graftsIL-1 receptorActive IL-1βCultured human endothelial cellsNLRP3 inflammasome assemblyNoncanonical NF-κBArtery graftAlloreactive CD8Complement membrane attack complexMemory CD4Advances in Disease Mechanisms and Translational Technologies: Clinicopathologic Significance of Inflammasome Activation in Autoimmune Diseases
Kahlenberg JM, Kang I. Advances in Disease Mechanisms and Translational Technologies: Clinicopathologic Significance of Inflammasome Activation in Autoimmune Diseases. Arthritis & Rheumatology 2020, 72: 386-395. PMID: 31562704, PMCID: PMC7050400, DOI: 10.1002/art.41127.Peer-Reviewed Original ResearchConceptsPattern recognition receptorsInflammasome activationRheumatic diseasesAutoimmune diseasesIL-18IL-1βClinicopathologic significanceProcaspase-1Damage-associated molecular patternsSystemic lupus erythematosusAdaptive immune pathwaysCrystal-induced arthropathiesCytokines IL-1βDevelopment of inflammationLocal inflammatory responseHost immune responsePrimary target organActive IL-1βActive caspase-1Inflammatory damageLupus erythematosusImmune toleranceRheumatoid arthritisSjögren's syndromePathogenic role
2011
Uric Acid Induces Trophoblast IL‐1β Production Via the Inflammasome: Implications for the Pathogenesis of Preeclampsia
Mulla MJ, Myrtolli K, Potter J, Boeras C, Kavathas PB, Sfakianaki AK, Tadesse S, Norwitz ER, Guller S, Abrahams VM. Uric Acid Induces Trophoblast IL‐1β Production Via the Inflammasome: Implications for the Pathogenesis of Preeclampsia. American Journal Of Reproductive Immunology 2011, 65: 542-548. PMID: 21352397, PMCID: PMC3114103, DOI: 10.1111/j.1600-0897.2010.00960.x.Peer-Reviewed Original ResearchMeSH KeywordsAdaptor Proteins, Signal TransducingApoptosis Regulatory ProteinsCARD Signaling Adaptor ProteinsCarrier ProteinsCaspase 1Cell LineCytoskeletal ProteinsDisease ProgressionEnzyme ActivationFemaleGene Expression Regulation, DevelopmentalHumansHyperuricemiaInflammasomesInterleukin-1betaMaternal-Fetal RelationsNLR Family, Pyrin Domain-Containing 3 ProteinNLR ProteinsPre-EclampsiaPregnancyTrophoblastsUric AcidConceptsIL-1β secretionIL-1β productionMonosodium urateTrophoblast cellsUric acidFirst trimester trophoblast cellsAdverse pregnancy outcomesPathogenesis of preeclampsiaMaternal-fetal interfaceInduction of inflammationActive IL-1βNOD-like receptorsThird trimester trophoblastActive caspase-1Uric acid increasesCaspase-1 activationIL-1β processingPregnancy outcomesInflammatory dysregulationPlacental dysfunctionClinical manifestationsIL-1βInflammasome activationNALP3 inflammasomePreeclampsia
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