2001
Resident and Infiltrating Central Nervous System APCs Regulate the Emergence and Resolution of Experimental Autoimmune Encephalomyelitis
Juedes A, Ruddle N. Resident and Infiltrating Central Nervous System APCs Regulate the Emergence and Resolution of Experimental Autoimmune Encephalomyelitis. The Journal Of Immunology 2001, 166: 5168-5175. PMID: 11290800, DOI: 10.4049/jimmunol.166.8.5168.Peer-Reviewed Original ResearchMeSH KeywordsAmino Acid SequenceAnimalsAntigen PresentationAntigen-Presenting CellsB7-1 AntigenBrainCell LineCell MovementDown-RegulationEncephalomyelitis, Autoimmune, ExperimentalFemaleGrowth InhibitorsHistocompatibility Antigens Class IHistocompatibility Antigens Class IILymphocyte ActivationMacromolecular SubstancesMacrophagesMiceMice, Inbred C57BLMice, KnockoutMicrogliaMolecular Sequence DataMyelin ProteinsMyelin-Associated GlycoproteinMyelin-Oligodendrocyte GlycoproteinNitric OxideSpinal CordT-LymphocytesConceptsExperimental autoimmune encephalomyelitisT cell proliferationT cellsT cell linesCNS APCCNS APCsAutoimmune encephalomyelitisMHC-IITarget organsInducible NO synthase-deficient miceT cell cytokine productionTh1 T cellsAutoreactive T cellsCell cytokine productionIFN-gamma productionB7-1 expressionSynthase-deficient miceCell proliferationMac-1 cellsCell linesInitiation of diseaseProduction of NOResident microgliaMyelin oligodendrocyteCytokine production
1997
Role of CD4+ T cells in pathogenesis associated with Leishmania amazonensis infection.
Soong L, Chang CH, Sun J, Longley BJ, Ruddle NH, Flavell RA, McMahon-Pratt D. Role of CD4+ T cells in pathogenesis associated with Leishmania amazonensis infection. The Journal Of Immunology 1997, 158: 5374-83. PMID: 9164958, DOI: 10.4049/jimmunol.158.11.5374.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsCD4-Positive T-LymphocytesDNA-Binding ProteinsHistocompatibility Antigens Class IIImmunity, CellularLeishmaniaLeishmaniasisMiceMice, Inbred C57BLProteinsConceptsII-/- miceLeishmania amazonensis infectionRag2-/- miceT cellsAmazonensis infectionMHC classL. amazonensis-infected miceWild-type C57BL/6 miceLarge ulcerating lesionsMonocytes/granulocytesRole of CD4Course of infectionMonocytes/macrophagesStrains of miceMHC class IWild-type CD4T cell developmentUlcerating lesionFunctional CD4Lymphocyte subsetsC57BL/6 miceTh1 cellsInflammatory responseLesion pathologyImmune response
1993
Transgenic tumor necrosis factor (TNF)-alpha production in pancreatic islets leads to insulitis, not diabetes. Distinct patterns of inflammation in TNF-alpha and TNF-beta transgenic mice.
Picarella DE, Kratz A, Li CB, Ruddle NH, Flavell RA. Transgenic tumor necrosis factor (TNF)-alpha production in pancreatic islets leads to insulitis, not diabetes. Distinct patterns of inflammation in TNF-alpha and TNF-beta transgenic mice. The Journal Of Immunology 1993, 150: 4136-50. PMID: 7682590, DOI: 10.4049/jimmunol.150.9.4136.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, SurfaceCD4 AntigensCD8 AntigensCell Adhesion MoleculesDiabetes Mellitus, Type 1Histocompatibility Antigens Class IIHumansIntercellular Adhesion Molecule-1Islets of LangerhansKidneyLeukocyte Common AntigensLymphotoxin-alphaMiceMice, Inbred NODMice, TransgenicPancreatitisProtein Tyrosine Phosphatase, Non-Receptor Type 1Receptors, Interleukin-2Tumor Necrosis Factor-alphaUp-RegulationConceptsTNF-alphaTransgenic miceTNF-alpha transgenic miceInsulin-dependent diabetes mellitusAdhesion molecules VCAM-1Rat insulin II promoterTNF-alpha transgeneRole of TNFMurine TNF-alphaTumor necrosis factorRegulation of inflammationMHC class IReduced insulin contentPeri-insulitisIslet destructionDiabetes mellitusAutoimmune diseasesAlpha productionIslet endotheliumNecrosis factorT cellsICAM-1VCAM-1Insulin contentB cells