grant
A TCF1:Glucocorticoid regulatory circuit controls IL-23-driven Th17 pathogenicity
Organization BRIGHAM AND WOMEN'S HOSPITALLocation BOSTON, UNITED STATESPosted 1 Feb 2023Deadline 31 Jan 2028
NIHUS FederalResearch GrantFY2025AnabolismAutomobile DrivingAutoregulationBeta Cadherin-Associated ProteinBeta-1 CateninBiologyBody TissuesBypassCNS DiseasesCNS Nervous SystemCNS autoimmunityCNS disorderCTLA-8CTLA-8 GeneCTLA8CTLA8 GeneCUL-2Cell BodyCell Communication and SignalingCell SignalingCellsCentral Nervous SystemCentral Nervous System DiseasesCentral Nervous System DisordersCytotoxic T-Lymphocyte-Associated Antigen 8Cytotoxic T-Lymphocyte-Associated Antigen 8 GeneCytotoxic T-Lymphocyte-Associated Serine Esterase 8Cytotoxic T-Lymphocyte-Associated Serine Esterase 8 GeneDataDefectDevelopmentDiathesisDiseaseDisease susceptibilityDisorderDisseminated SclerosisEnzyme GeneEnzymesEpigeneticEpigenetic ChangeEpigenetic MechanismEpigenetic ProcessGM-CSFGWA studyGWASGene DeletionGene TranscriptionGene variantGenesGenetic DiversityGenetic TranscriptionGenetic VariationGerm LinesGlucocorticoid ReceptorGlucocorticoidsGranulocyte-Macrophage Colony-Stimulating FactorHelper CellsHelper T-CellsHelper T-LymphocytesHelper-Inducer T-CellsHelper-Inducer T-LymphocyteHistamine-Producing Cell-Stimulating FactorHomeostasisHumanIL-17IL-17 GeneIL-17AIL-17A GeneIL-23IL17IL17 ProteinIL17 geneIL17AIL17A GeneImpairmentInducer CellsInducer T-LymphocytesInflammationInflammatoryInterleukin 17 (Cytotoxic T-Lymphocyte-Associated Serine Esterase 8)Interleukin 17 (Cytotoxic T-Lymphocyte-Associated Serine Esterase 8) GeneInterleukin 17 PrecursorInterleukin 17 Precursor GeneInterleukin-17Intracellular Communication and SignalingInvestigationKO miceKnock-out MiceKnockout MiceKnowledgeLEF Transcription FactorLinkLymphoid Enhancer FactorMature T-CellMature T-LymphocyteMediatingMediatorMiceMice MammalsModelingModern ManMolgramostinMultiple SclerosisMurineMusNeuraxisNull MousePRO2286PathogenicityPatientsPhysiological HomeostasisPredispositionPrevalenceRNA ExpressionRegulationRelapseRelapsing-Remitting Multiple SclerosisRoleSignal TransductionSignal Transduction SystemsSignalingSteroid biosynthesisSusceptibilityT Cell FactorT-Cell DevelopmentT-Cell OntogenyT-CellsT-LymphocyteT-Lymphocyte DevelopmentTC-GM-CSFTCF Transcription FactorTestingThymocyte SelectionTissuesTranscriptionTumor-Cell Human GM Colony-Stimulating Factorallelic variantautoimmune inflammationbeta catbeta cateninbiological signal transductionbiosynthesiscentral nervous system autoimmunityclinical relevanceclinically relevantconditional knock-outconditional knockoutdevelopmentaldrivingepigeneticallyepigenomegene deletion mutationgenetic variantgenome wide associationgenome wide association scangenome wide association studygenomewide association scangenomewide association studygenomic variantglobal gene expressionglobal transcription profilein vivoinsightinsular sclerosisinterleukin-23liability to diseasenew therapeutic approachnew therapeutic interventionnew therapeutic strategiesnew therapy approachesnew treatment approachnew treatment strategynovelnovel therapeutic approachnovel therapeutic interventionnovel therapeutic strategiesnovel therapy approachprogramsrestraintsocial rolesteroidogenesisthymus derived lymphocytetooltranscriptomewhole genome association analysiswhole genome association studyβ-catenin
Description preview
PROJECT SUMMARY
CD4+ IL-17-producing T helper cells (Th17) are known drivers of central nervous system (CNS) autoimmune
inflammation in multiple sclerosis (MS), yet not all Th17 cells drive disease. Indeed, two major Th17 subtypes
have been described in both mice and humans: homeostatic or non-pathogenic (npTh17) that maintain the
steady state in…
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