grant
Mechanisms of T cell persistence during chronic autoimmunity
Organization UTAH STATE HIGHER EDUCATION SYSTEM--UNIVERSITY OF UTAHLocation SALT LAKE CITY, UNITED STATESPosted 1 Dec 2023Deadline 31 Oct 2028
NIHUS FederalResearch GrantFY2026AddressAffinityAntigenic DeterminantsAntigensAutoantigensAutoimmuneAutoimmune DiabetesAutoimmune StatusAutoimmunityAutologous AntigensB9 endocrine pancreasBasal Transcription FactorBasal transcription factor genesBeta CellBinding DeterminantsBiological MarkersBody TissuesBrittle Diabetes MellitusCD3CD3 AntigensCD3 ComplexCD3 moleculeCD4 CellsCD4 Positive T LymphocytesCD4 T cellsCD4 helper T cellCD4 lymphocyteCD4+ T-LymphocyteCD4-Positive LymphocytesCD62LCD8 CellCD8 T cellsCD8 lymphocyteCD8+ T cellCD8+ T-LymphocyteCD8-Positive LymphocytesCD8-Positive T-LymphocytesCausalityCell BodyCell Communication and SignalingCell CountCell NumberCell SignalingCellsChromatinChronicChronic DiseaseChronic IllnessDataDevelopmentDiabetes MellitusDiseaseDisease remissionDisorderEndocrine PancreasEpigeneticEpigenetic ChangeEpigenetic MechanismEpigenetic ProcessEpitopesEtiologyExhibitsExpression SignatureFilamentous FungiGene Expression ProfileGene TranscriptionGeneral Transcription Factor GeneGeneral Transcription FactorsGenetic TranscriptionHLHRCHeterogeneityHumulin RIDDMImmune Cell ActivationImmune responseImmunotherapeutic agentInbred NOD MiceInfiltrationInflammationInsulinInsulin CellInsulin Secreting CellInsulin-Dependent Diabetes MellitusIntracellular Communication and SignalingIslands of LangerhansIslets of LangerhansJuvenile-Onset Diabetes MellitusKetosis-Prone Diabetes MellitusKnowledgeLAM-1 geneLECAM1LNHRLSELLYAM-1LYAM1MHC ReceptorMaintenanceMajor Histocompatibility Complex ReceptorMeasurementMediatingMemoryMethylationMiceMice MammalsMoldsMurineMusMutant Strains MiceNOD MouseNesidioblastsNon-Obese Diabetic MiceNonobese Diabetic MouseNovolin ROKT3 antigenPancreasPancreaticPancreatic IsletsPars endocrina pancreatisPathogenicityPeripheralPhenotypePopulationPredispositionProgenitor CellsRNA ExpressionRegular InsulinRegulationRemissionResistanceRoleSELL geneSelectin L GeneSelf-AntigensSignal TransductionSignal Transduction SystemsSignalingSiteSourceStem Cell likeSudden-Onset Diabetes MellitusSusceptibilityT cell infiltrationT cell responseT memory cellT-Cell Antigen ReceptorsT-Cell ReceptorT-CellsT-LymphocyteT1 DMT1 diabetesT1DT1DMT3 AntigensT3 ComplexT3 moleculeT4 CellsT4 LymphocytesT8 CellsT8 LymphocytesTQ-1TestingTissuesTranscriptionTranscription Factor Proto-OncogeneTranscription factor genesTranscriptional ControlTranscriptional RegulationType 1 Diabetes MellitusType 1 diabetesType I Diabetes MellitusWorkautoimmune reactivityautoreactive T cellautoreactivitybio-markersbiologic markerbiological signal transductionbiomarkercausationchronic disorderdevelopmentaldiabetesdisease causationentire genomeepigenetic regulationepigeneticallyexhaustionexperiencefull genomegene expression patterngene expression signaturehost responseimmune activationimmune drugsimmune system responseimmune-based therapeuticsimmunogenimmunologic therapeuticsimmunoresponseimmunotherapeuticsimmunotherapy agentimprovedinsulin dependent diabetesinsulin dependent type 1isletjuvenile diabetesjuvenile diabetes mellitusketosis prone diabetesloss of functionmemory T lymphocytemouse mutantnon-obese diabetic (NOD) micenonobese diabetic (NOD) micepathogenprogenitor capacityprogenitor cell likeprogenitor-likerecruitresistantresponserestraintself-reactive T cellself-renewself-renewalsocial rolestem cell characteristicsstem cellsstem-likestemnessthymus derived lymphocytetooltraffickingtranscription factortranscriptional profiletranscriptional signaturetype I diabetestype one diabeteswhole genomeβ-cellβ-cellsβCell
Description preview
PROJECT SUMMARY/ABSTRACT
Chronic stimulation depletes memory T cell potential and leads to exhaustion. However, self-reactive
autoimmune T cell responses persist and maintain function during chronic autoimmunity. The mechanisms
behind persistence of autoimmune T cells, including resistance to regulatory mechanisms such as deletion and
exhaustion,…
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