2008
CTLA4Ig treatment in patients with multiple sclerosis
Viglietta V, Bourcier K, Buckle GJ, Healy B, Weiner HL, Hafler DA, Egorova S, Guttmann CR, Rusche JR, Khoury SJ. CTLA4Ig treatment in patients with multiple sclerosis. Neurology 2008, 71: 917-924. PMID: 18794494, DOI: 10.1212/01.wnl.0000325915.00112.61.Peer-Reviewed Original ResearchConceptsMultiple sclerosisCostimulatory pathwayPhase 1 dose-escalation studyT cell-mediated autoimmune diseaseCell-mediated autoimmune diseaseRelapsing-remitting multiple sclerosisT-cell costimulatory pathwaysCostimulatory molecule interactionsMonths of infusionDose-escalation studyInterferon-gamma productionT cell activationOriginal therapeutic approachAdverse eventsImmunologic assessmentImmunologic effectsCTLA4Ig treatmentChronic inflammationAutoimmune diseasesInflammatory processT cellsImmune responseTherapeutic approachesCTLA4IgExtension study
1999
The B7–CD28/CTLA-4 costimulatory pathways in autoimmune disease of the central nervous system
Anderson D, Sharpe A, Hafler D. The B7–CD28/CTLA-4 costimulatory pathways in autoimmune disease of the central nervous system. Current Opinion In Immunology 1999, 11: 677-683. PMID: 10631554, DOI: 10.1016/s0952-7915(99)00036-9.Peer-Reviewed Original ResearchConceptsSelf-reactive T cellsB7-CD28/CTLAAutoimmune diseasesT cellsTh1/Th2 cell differentiationB7-CD28 costimulationHuman autoimmune diseasesCentral nervous systemTh2 cell differentiationCostimulatory pathwayEffector phaseCTLA-4Nervous systemCritical roleDiseaseCTLARecent studiesCell differentiationCellsPast yearPathwayAutoimmunityCD28InitiationCostimulationMolecular pathogenesis of multiple sclerosis
Bar-Or A, Oliveira E, Anderson D, Hafler D. Molecular pathogenesis of multiple sclerosis. Journal Of Neuroimmunology 1999, 100: 252-259. PMID: 10695735, DOI: 10.1016/s0165-5728(99)00193-9.Peer-Reviewed Original ResearchConceptsMultiple sclerosisT cellsMyelin-reactive T cellsCentral nervous system white matterB7 costimulatory pathwayNervous system white matterDifferential activation statesMacrophage infiltratesMS patientsAxonal injuryNeurological functionProinflammatory cellsProinflammatory cytokinesCostimulatory pathwayInflammatory diseasesMS lesionsMolecular pathogenesisWhite matterMolecular mimicryMatrix metalloproteinasesNormal individualsAdhesion moleculesSelective expressionSclerosisActivation state