2005
Chronic Lymphocytic Inflammation Specifies the Organ Tropism of Prions
Heikenwalder M, Zeller N, Seeger H, Prinz M, Klöhn P, Schwarz P, Ruddle NH, Weissmann C, Aguzzi A. Chronic Lymphocytic Inflammation Specifies the Organ Tropism of Prions. Science 2005, 307: 1107-1110. PMID: 15661974, DOI: 10.1126/science.1106460.Peer-Reviewed Original ResearchConceptsInflammatory conditionsNormal cellular prion protein PrPCCellular prion protein PrPCChronic lymphocytic inflammationIatrogenic prion transmissionChronic inflammatory conditionsPrion protein PrPCFDC-M1Lymphocytic inflammationEctopic inductionProinflammatory cytokinesInflamed organsImmune cellsInflammatory diseasesInflammatory fociLymphoid tissuePrion accumulationPrion inoculationOrgan tropismPrion pathogenesisPrion replicationTissue distributionPrion transmissionPrionsMice
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
1996
The Contribution of Insulitis to Diabetes Development in Tumor Necrosis Factor Transgenic Mice
Flavell RA, Kratz A, Ruddle NH. The Contribution of Insulitis to Diabetes Development in Tumor Necrosis Factor Transgenic Mice. Current Topics In Microbiology And Immunology 1996, 206: 33-50. PMID: 8608724, DOI: 10.1007/978-3-642-85208-4_3.Peer-Reviewed Original ResearchConceptsInsulin-dependent diabetes mellitusTumor necrosis factor-transgenic (TNF-Tg) miceDevelopment of diabetesHLA susceptibility allelesIslets of LangerhansHLA-DQβDiabetes mellitusFrank diabetesTransgenic miceStrong associationSusceptibility allelesDiabetesIdentical twinsDiseaseInsulinIsletsInsulitisSite of synthesisMellitusNumber of yearsPatientsMiceEnvironmental factors
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