2020
The receptor for advanced glycation endproducts (RAGE) modulates T cell signaling
Reed JC, Preston-Hurlburt P, Philbrick W, Betancur G, Korah M, Lucas C, Herold KC. The receptor for advanced glycation endproducts (RAGE) modulates T cell signaling. PLOS ONE 2020, 15: e0236921. PMID: 32986722, PMCID: PMC7521722, DOI: 10.1371/journal.pone.0236921.Peer-Reviewed Original ResearchConceptsT cellsAdvanced glycation endproductsRAGE expressionGlycation endproductsType 1 diabetes mellitusLess IL-2T cell reactivityT-cell phenotypeHealthy control subjectsIL-2 productionT cell receptorPhosphorylation of ZAP70Human T cellsDiabetes mellitusAutoimmune diseasesJurkat cellsCell reactivityControl subjectsInflammatory productsIL-2Primary CD4T cell signalingCell receptorPatientsCell phenotype
2015
Cross‐reactivity of Gut Commensals and Autoantigen in Antiphospholipid Syndrome
Dehner C, Ruff W, Vieira S, Goodman A, Kriegel M. Cross‐reactivity of Gut Commensals and Autoantigen in Antiphospholipid Syndrome. The FASEB Journal 2015, 29 DOI: 10.1096/fasebj.29.1_supplement.142.4.Peer-Reviewed Original ResearchAntiphospholipid syndromeMemory T cellsAutoimmune disease modelsGut commensalsAdaptive immune responsesB cell reactivityB-cell epitopesPatient plasma samplesAPS pathogenesisAPS patientsPatient PBMCsUnknown etiologyCell reactivityControl subjectsT cellsImmune responseCell epitopesT cell librariesB cellsGut microbiotaWestern blot experimentsWestern blottingHuman autoantigensDisease modelsPlasma samples
2005
High Incidence of Spontaneous Disease in an HLA-DR15 and TCR Transgenic Multiple Sclerosis Model
Ellmerich S, Mycko M, Takacs K, Waldner H, Wahid FN, Boyton RJ, King RH, Smith PA, Amor S, Herlihy AH, Hewitt RE, Jutton M, Price DA, Hafler DA, Kuchroo VK, Altmann DM. High Incidence of Spontaneous Disease in an HLA-DR15 and TCR Transgenic Multiple Sclerosis Model. The Journal Of Immunology 2005, 174: 1938-1946. PMID: 15699121, DOI: 10.4049/jimmunol.174.4.1938.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigen PresentationCell MovementCentral Nervous SystemDisease Models, AnimalDisease ProgressionDNA-Binding ProteinsEpitopes, T-LymphocyteHLA-DR AntigensHLA-DR Serological SubtypesMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicMultiple SclerosisMyelin Basic ProteinParalysisPeptide FragmentsReceptors, Antigen, T-Cell, alpha-betaT-Lymphocyte SubsetsConceptsT cell responsesHLA-DR15Multiple sclerosisDeterminant spreadSpontaneous diseaseCell responsesCD4 T cell recognitionCNS tissue damageHuman multiple sclerosisMultiple sclerosis modelT cell reactivityExperimental allergic encephalomyelitisMyelin oligodendrocyte glycoproteinT cell recognitionMyelin basic proteinAllergic encephalomyelitisMyelin epitopesPeptide immunotherapyAxonal degenerationCell reactivityOligodendrocyte glycoproteinPathogenic roleT cellsHigh incidenceTransgenic mice
2004
Leishmanial Amastigote Antigen P‐2 Induces Major Histocompatibility Complex Class II‐Dependent Natural Killer‐Cell Reactivity in Cells from Healthy Donors
Nylén S, Maasho K, McMahon‐Pratt D, Akuffo H. Leishmanial Amastigote Antigen P‐2 Induces Major Histocompatibility Complex Class II‐Dependent Natural Killer‐Cell Reactivity in Cells from Healthy Donors. Scandinavian Journal Of Immunology 2004, 59: 294-304. PMID: 15030581, DOI: 10.1111/j.0300-9475.2004.01388.x.Peer-Reviewed Original ResearchMeSH KeywordsAnimalsAntigens, ProtozoanCD8-Positive T-LymphocytesFetal BloodHistocompatibility Antigens Class IIHumansInterferon-gammaInterleukin-10Killer Cells, NaturalLeishmaniaLeishmaniasisLymphocyte ActivationProtozoan VaccinesReceptors, IgGReverse Transcriptase Polymerase Chain ReactionRNA, MessengerConceptsHealthy donorsLeishmaniasis patientsAmerican cutaneous leishmaniasis patientsClass IIMajor histocompatibility complex class IIMajor histocompatibility complex classHistocompatibility complex class IIClass II antibodiesCutaneous leishmaniasis patientsInterleukin-10 productionNatural killer cellsProtective immune responseInterferon-gamma productionIFN-gamma responsesMHC class IIHistocompatibility complex classHealthy adult donorsDevelopment of vaccinesAdherent cell populationAmastigote antigensNatural killerKiller cellsCytokine productionCell reactivityLeishmania infection
2003
In vitro evidence that subcutaneous administration of glatiramer acetate induces hyporesponsive T cells in patients with multiple sclerosis
Schmied M, Duda PW, Krieger JI, Trollmo C, Hafler DA. In vitro evidence that subcutaneous administration of glatiramer acetate induces hyporesponsive T cells in patients with multiple sclerosis. Clinical Immunology 2003, 106: 163-174. PMID: 12706402, DOI: 10.1016/s1521-6616(03)00020-2.Peer-Reviewed Original ResearchConceptsGA-reactive T cellsT cell reactivityT cellsRR-MSMultiple sclerosisCell reactivityT cell peripheral toleranceTh2-type T cellsT cell frequenciesMonths of treatmentT cell hyporesponsivenessT cell populationsT cell nonresponsivenessT cell anergyHyporesponsive T cellsMechanism of actionMyelin antigensGlatiramer acetatePeripheral toleranceCell hyporesponsivenessPeripheral bloodClonal eliminationIL-2Cell anergySubcutaneous administration
2001
Type 1 Diabetes-Predisposing MHC Alleles Influence the Selection of Glutamic Acid Decarboxylase (GAD) 65-Specific T Cells in a Transgenic Model
Abraham R, Wen L, Marietta E, David C. Type 1 Diabetes-Predisposing MHC Alleles Influence the Selection of Glutamic Acid Decarboxylase (GAD) 65-Specific T Cells in a Transgenic Model. The Journal Of Immunology 2001, 166: 1370-1379. PMID: 11145722, DOI: 10.4049/jimmunol.166.2.1370.Peer-Reviewed Original ResearchMeSH KeywordsAllelesAmino Acid SequenceAnimalsAntibody SpecificityCells, CulturedCytokinesDiabetes Mellitus, Type 1Disease Models, AnimalEpitopes, T-LymphocyteGenes, MHC Class IIGenetic Predisposition to DiseaseGlutamate DecarboxylaseHLA-DQ AntigensHLA-DR3 AntigenHumansImmunophenotypingIslets of LangerhansIsoenzymesLymphocyte ActivationMiceMice, Inbred C57BLMice, TransgenicMolecular Sequence DataRatsT-Lymphocyte SubsetsConceptsGlutamic acid decarboxylaseGAD 65T cellsDQ8 miceMixed Th1/Th2 cytokine profileEndogenous MHC class IISpontaneous T-cell reactivityTh1/Th2 cytokine profileGlutamic acid decarboxylase 65Self-reactive responsesT cell reactivityTh2 cytokine profileAutoantigen glutamic acid decarboxylase 65Type 1 diabetesMHC class IIDiabetes-associated genesCytokine profileIslet autoantigensHLA-DR3Immune toleranceHLA-DQ6Cell reactivitySelf-AgImmune responseHLA alleles
1987
Myelin basic protein and proteolipid protein reactivity of brain- and cerebrospinal fluid-derived T cell clones in multiple sclerosis and postinfectious encephalomyelitis.
Hafler DA, Benjamin DS, Burks J, Weiner HL. Myelin basic protein and proteolipid protein reactivity of brain- and cerebrospinal fluid-derived T cell clones in multiple sclerosis and postinfectious encephalomyelitis. The Journal Of Immunology 1987, 139: 68-72. PMID: 2438352, DOI: 10.4049/jimmunol.139.1.68.Peer-Reviewed Original ResearchConceptsT cell clonesMyelin basic proteinPeripheral bloodPostinfectious encephalomyelitisCell clonesMultiple sclerosisT cellsProteolipid proteinPeripheral blood T cell clonesBlood T-cell clonePlaque tissueMS plaque tissueProportion of T4T cell reactivityHuman myelin basic proteinBasic proteinMS patientsCell reactivityIL-2Cerebrospinal fluidTarget antigenClear reactivityBrain tissueBloodEncephalomyelitis
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