2001
Lymphotoxin-alpha deficiency completely protects C57BL/6 mice from developing clinical experimental autoimmune myasthenia gravis
Goluszko E, Hjelmström P, Deng C, Poussin M, Ruddle N, Christadoss P. Lymphotoxin-alpha deficiency completely protects C57BL/6 mice from developing clinical experimental autoimmune myasthenia gravis. Journal Of Neuroimmunology 2001, 113: 109-118. PMID: 11137582, DOI: 10.1016/s0165-5728(00)00420-3.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CDAutoantibodiesB7-2 AntigenGene ExpressionImmunodominant EpitopesImmunoglobulin GImmunoglobulin MLymphotoxin-alphaMembrane GlycoproteinsMiceMice, Inbred C57BLMice, KnockoutMyasthenia Gravis, Autoimmune, ExperimentalReceptors, CholinergicReceptors, Tumor Necrosis FactorSpleenConceptsExperimental autoimmune myasthenia gravisClinical experimental autoimmune myasthenia gravisAutoimmune myasthenia gravisMyasthenia gravisMean titersPrimary humoral immune responseAlpha-deficient miceAnti-AChR antibodiesHumoral immune responseLower mean titersC57BL/6 miceImmunized miceTotal IgGDeficient miceIgG isotypeImmune responseAcetylcholine receptorsPartial preventionGravisMiceComplete preventionTitersLtPreventionPathogenesisICOS co-stimulatory receptor is essential for T-cell activation and function
Dong C, Juedes A, Temann U, Shresta S, Allison J, Ruddle N, Flavell R. ICOS co-stimulatory receptor is essential for T-cell activation and function. Nature 2001, 409: 97-101. PMID: 11343121, DOI: 10.1038/35051100.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsAntibody FormationAntigens, CDAntigens, Differentiation, T-LymphocyteCell DifferentiationCells, CulturedEncephalomyelitis, Autoimmune, ExperimentalGene TargetingHemocyaninsInducible T-Cell Co-Stimulator ProteinInterleukin-13Interleukin-4Lymph NodesLymphocyte ActivationMiceMice, KnockoutMolecular Sequence DataMyelin ProteinsMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinT-LymphocytesConceptsInducible co-stimulatory moleculeT cell activationCo-stimulatory moleculesT cellsICOS-/- miceICOS-deficient miceInflammatory autoimmune diseaseExperimental autoimmune encephalomyelitisInjection of lipopolysaccharideCo-stimulatory receptorsHumoral immune responseNon-immune tissuesT lymphocyte activationAutoimmune encephalomyelitisAutoimmune diseasesImmune responseInterleukin-4Immune functionCD28/CTLA4 familyB cellsProtective roleEnhanced susceptibilityActivationReceptorsHigh affinity
2000
Lymphoid Tissue Homing Chemokines Are Expressed in Chronic Inflammation
Hjelmström P, Fjell J, Nakagawa T, Sacca R, Cuff C, Ruddle N. Lymphoid Tissue Homing Chemokines Are Expressed in Chronic Inflammation. American Journal Of Pathology 2000, 156: 1133-1138. PMID: 10751336, PMCID: PMC1876894, DOI: 10.1016/s0002-9440(10)64981-4.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, CDChemokine CCL21Chemokine CXCL13Chemokines, CCChemokines, CXCChronic DiseaseFemaleInflammationLymphotoxin-alphaLymphotoxin-betaMembrane ProteinsMiceMice, Inbred NODMice, TransgenicPancreasPancreatitisProtein IsoformsReceptors, Tumor Necrosis FactorReceptors, Tumor Necrosis Factor, Type IRNA, MessengerConceptsSecondary lymphoid tissue chemokineB lymphocyte chemoattractantExpression of SLCChronic inflammationLymphoid organsPrediabetic nonobese diabetic (NOD) micePrediabetic NOD miceLymphoid tissue chemokineNonobese diabetic (NOD) miceChronic inflammatory diseaseSecondary lymphoid organsTrafficking of lymphocytesTumor necrosis factor receptor 1Necrosis factor receptor 1Factor receptor 1Homing ChemokinesLymphocyte chemoattractantLymphoid neogenesisNOD miceDendritic cellsDiabetic miceInflammatory diseasesInflammatory processLymphoid tissueInflamed tissues