1998
Identification of a T cell subset capable of both IFN-gamma and IL-10 secretion in patients with chronic Borrelia burgdorferi infection.
Pohl-Koppe A, Balashov K, Steere A, Logigian E, Hafler D. Identification of a T cell subset capable of both IFN-gamma and IL-10 secretion in patients with chronic Borrelia burgdorferi infection. The Journal Of Immunology 1998, 160: 1804-10. PMID: 9469440, DOI: 10.4049/jimmunol.160.4.1804.Peer-Reviewed Original ResearchConceptsT cell linesIFN-gamma/ILB. burgdorferi infectionIFN-gammaBurgdorferi infectionT cellsIL-12Lyme patientsCell linesLyme diseaseVigorous humoral immune responseIL-10 secretionExogenous IL-12T cell subsetsT cell populationsHumoral immune responseNovel populationB. burgdorferiBorrelia burgdorferi infectionPrecursor T cellsWhole mononuclear cellsHuman T cellsGroups of subjectsIL-10Cell subsets
1992
T cell receptor V alpha-V beta repertoire and cytokine gene expression in active multiple sclerosis lesions.
Wucherpfennig KW, Newcombe J, Li H, Keddy C, Cuzner ML, Hafler DA. T cell receptor V alpha-V beta repertoire and cytokine gene expression in active multiple sclerosis lesions. Journal Of Experimental Medicine 1992, 175: 993-1002. PMID: 1348083, PMCID: PMC2119186, DOI: 10.1084/jem.175.4.993.Peer-Reviewed Original ResearchMeSH KeywordsAcute DiseaseAntigens, Differentiation, T-LymphocyteBase SequenceCD2 AntigensChronic DiseaseClone CellsCytokinesGene ExpressionHumansInterleukin-1Interleukin-2Interleukin-4Molecular Sequence DataMultiple SclerosisOligodeoxyribonucleotidesPolymerase Chain ReactionReceptors, Antigen, T-Cell, alpha-betaReceptors, ImmunologicRNA, MessengerConceptsTCR V alphaTCR repertoireBeta repertoireMultiple sclerosisV alphaActive lesionsMS plaquesT cellsAlpha/beta T cellsActive multiple sclerosis lesionsMS plaque tissueCentral nervous system tissueT cell recruitmentBeta T cellsActive MS plaquesChronic inflammatory diseaseIL-4 mRNAT cell expansionIL-1 mRNATCR V gene segmentsCentral nervous systemCases of subacuteNervous system tissueSites of inflammationTCR V genes
1991
Tolerance and suppressor mechanisms in experimental autoimmune encephalomyelitis: implications for immunotherapy of human autoimmune diseases
Miller A, Hafler D, Weiner H. Tolerance and suppressor mechanisms in experimental autoimmune encephalomyelitis: implications for immunotherapy of human autoimmune diseases. The FASEB Journal 1991, 5: 2560-2566. PMID: 1868980, DOI: 10.1096/fasebj.5.11.1868980.Peer-Reviewed Original ResearchConceptsExperimental autoimmune encephalomyelitisAutoimmune encephalomyelitisAutoimmune diseasesAnimal model experimental autoimmune encephalomyelitisModel experimental autoimmune encephalomyelitisHuman disease multiple sclerosisSpecific immune interventionAutoimmune T cellsHuman autoimmune diseasesNormal immune systemDisease multiple sclerosisMajor histocompatibility complexImmunospecific therapyTrimolecular complexImmune interventionSelective immunotherapyMultiple sclerosisT cellsImmune functionNonspecific modulationImmune systemAntigen recognitionHistocompatibility complexSuppressor mechanismDisease
1988
The 2H4 (CD45R) antigen is selectively decreased in multiple sclerosis lesions.
Sobel RA, Hafler DA, Castro EE, Morimoto C, Weiner HL. The 2H4 (CD45R) antigen is selectively decreased in multiple sclerosis lesions. The Journal Of Immunology 1988, 140: 2210-4. PMID: 2965183, DOI: 10.4049/jimmunol.140.7.2210.Peer-Reviewed Original ResearchConceptsMultiple sclerosisViral encephalitisImmune responseCentral nervous system immune responseSuppressor-inducer functionCentral nervous system tissuePlaque edgeAdjacent white matterIL-2R mAbNervous system tissueMultiple sclerosis lesionsAnti-2H4Anti-CD4Inflammatory cellsMS plaquesImmunohistochemical stainingWhite matterSclerosis lesionsEncephalitisPatientsCellsRare cellsCD8CD4Sclerosis