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Modulation of pathogenic T cells in EAE
Organization BENAROYA RESEARCH INST AT VIRGINIA MASONLocation SEATTLE, UNITED STATESPosted 13 Nov 2023Deadline 31 Oct 2025 β οΈ
NIHUS FederalResearch GrantFY2025AddressAdoptive TransferAnimal ModelAnimal Models and Related StudiesAutoimmune DiseasesAutoimmune StatusAutoimmunityAutoregulationBasal Transcription FactorBasal transcription factor genesBody TissuesCD4 CellsCD4 Positive T LymphocytesCD4 T cellsCD4 helper T cellCD4 lymphocyteCD4+ T-LymphocyteCD4-Positive LymphocytesCNS Nervous SystemCNS autoimmunityCTLA-8CTLA-8 GeneCTLA8CTLA8 GeneCell BodyCell Communication and SignalingCell FunctionCell PhysiologyCell ProcessCell SignalingCellsCellular FunctionCellular PhysiologyCellular ProcessCentral Nervous SystemCharacteristicsChronicCo-StimulatorCostimulatorCytotoxic T-Lymphocyte-Associated Antigen 8Cytotoxic T-Lymphocyte-Associated Antigen 8 GeneCytotoxic T-Lymphocyte-Associated Serine Esterase 8Cytotoxic T-Lymphocyte-Associated Serine Esterase 8 GeneDataDemyelinationsDevelopmentDiseaseDisease ProgressionDisorderDisseminated SclerosisEAEEpidermal Thymocyte Activating FactorEquilibriumExperimental Allergic EncephalitisExperimental Allergic EncephalomyelitisExperimental Autoimmune EncephalitisExperimental Autoimmune EncephalomyelitisExpression SignatureFrequenciesGM-CSFGene Expression ProfileGeneral Transcription Factor GeneGeneral Transcription FactorsGeneralized GrowthGenetic studyGeographyGrantGranulocyte-Macrophage Colony-Stimulating FactorGrowthHistamine-Producing Cell-Stimulating FactorHomeostasisHuman GeneticsIFN-GammaIFN-gIFN-Ξ³IFNGIFNΞ³IL-17IL-17 GeneIL-17AIL-17A GeneIL-2IL17IL17 ProteinIL17 geneIL17AIL17A GeneIL2 ProteinImmune InterferonImmunityInflammationInterferon GammaInterferon Type IIInterleukin 17 (Cytotoxic T-Lymphocyte-Associated Serine Esterase 8)Interleukin 17 (Cytotoxic T-Lymphocyte-Associated Serine Esterase 8) GeneInterleukin 17 PrecursorInterleukin 17 Precursor GeneInterleukin 2Interleukin 2 PrecursorInterleukin IIInterleukin-17Interleukin-2Interleukine 2Interleukine 2 PrecursorInterleukine IIIntracellular Communication and SignalingLocationLymph Node Reticuloendothelial SystemLymph node properLymphatic nodesLymphocyte Mitogenic FactorMaintenanceMapsMiceMice MammalsMitogenic FactorModelingMolgramostinMultiple SclerosisMurineMusMyelinNerve DegenerationNeuraxisNeuron DegenerationOnset of illnessPathogenicityPathway interactionsPhasePhysiological HomeostasisPopulationProductionProliferatingPublishingRegulationRegulatory T-LymphocyteRemission InductionRoleSTAT1STAT1 geneSTAT91Signal TransductionSignal Transduction SystemsSignalingSourceSubcellular ProcessT cell growth factorT-Cell Growth FactorT-Cell Stimulating FactorT-CellsT-LymphocyteT4 CellsT4 LymphocytesTC-GM-CSFTestingThymocyte Stimulating FactorTissue GrowthTissuesTranscription Factor Proto-OncogeneTranscription factor genesTregTumor-Cell Human GM Colony-Stimulating Factorautoimmune conditionautoimmune disorderautoimmune encephalomyelitisautoimmunity diseasebalancebalance functionbiological signal transductionbiomarker identificationcentral nervous system autoimmunitycytokinedemyelinatedevelopmentaldisease onsetdisorder onsetexperimentexperimental researchexperimental studyexperimentsgene expression patterngene expression signatureidentification of biomarkersidentification of new biomarkersinsightinsular sclerosislFN-Gammalymph glandlymph nodeslymph organlymphatic organlymphnodeslymphoid organmarker identificationmodel of animalneural degenerationneurodegenerationneurodegenerativeneurological degenerationneuronal degenerationnovelontogenypathwaypreventpreventingrecruitregulatory T-cellsscRNA sequencingscRNA-seqsingle cell RNA-seqsingle cell RNAseqsingle cell expression profilingsingle cell transcriptomic profilingsingle-cell RNA sequencingsocial rolethymus derived lymphocytetooltranscription factortranscriptional profiletranscriptional signature
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Project Summary
Multiple sclerosis (MS) is a disease characterized by inflammation, demyelination, and neurodegeneration of the
central nervous system (CNS). Human genetic studies and adoptive transfer experiments in experimental
autoimmune encephalomyelitis (EAE), an animal model of MS point to CD4+ T helper cells as important actors
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