grant
Characterization of Mucosal Lymphocytes
Organization BRIGHAM AND WOMEN'S HOSPITALLocation BOSTON, UNITED STATESPosted 30 Sept 1992Deadline 30 Jun 2029
NIHUS FederalResearch GrantFY202521+ years oldAddressAdultAdult HumanAntibiotic TherapyAntibiotic TreatmentBirthBody TissuesBone Morphogenetic Protein GeneBone Morphogenetic ProteinsCancersCeliac DiseaseCeliac SprueCell BodyCell Communication and SignalingCell CountCell FunctionCell Growth in NumberCell MultiplicationCell NumberCell PhysiologyCell ProcessCell ProliferationCell SignalingCell-Mediated Lympholytic CellsCellsCellular FunctionCellular PhysiologyCellular ProcessCellular ProliferationCoeliac DiseaseColitisCollaborationsColonCytolytic T-CellCytotoxic T CellCytotoxic T-LymphocytesDevelopmentDiathesisDiseaseDisease susceptibilityDisorderEmbryoEmbryonicEmigrantEngraftmentEnteralEntericEosinophilic EsophagitisEsophageal DiseasesEsophageal DisorderEventGeographyGerm-FreeGluten EnteropathyGluten-Sensitive EnteropathyGoalsHumanImmuneImmune systemImmunesInfectionInflammatory Bowel DiseasesInflammatory Bowel DisorderIntestinalIntestinesIntracellular Communication and SignalingLamina PropriaLifeLong-Term EffectsLymphatic cellLymphocyteLymphocyticMacrophageMalignant NeoplasmsMalignant TumorMediatingMiceMice MammalsMicrobeMissionModern ManMolecularMucosaMucosal TissueMucous MembraneMurineMusMφNIDDKNK T cellNKT cellNational Institute of Diabetes and Digestive and Kidney DiseasesNatural Killer T cellNatureNeonatalNon-tropical SprueNontropical SprueOutcomeOxazoloneParturitionPathogenesisPathologyPathway interactionsPhenotypePlayPopulationPredispositionPublic HealthRegulationResearchResearch ProposalsResidenciesResistanceRoleSignal TransductionSignal Transduction SystemsSignalingSignaling Factor Proto-OncogeneSignaling Pathway GeneSignaling ProteinSmall IntestinesStromal CellsSubcellular ProcessSusceptibilityT-Cell ProliferationTestingThymusThymus GlandThymus ProperThymus Reticuloendothelial SystemTimeTissuesUlcerated ColitisUlcerative ColitisWeaningadulthoodbacterial disease treatmentbacterial infectious disease treatmentbiological signal transductionbone morphogenic proteinbowelcell typecommensal floracommensal microbescommensal microbiotacommensal microfloracritical developmental periodcritical perioddevelopmentaldiseases of esophagusenteral pathogenenteric pathogenenteropathogenesophagus disorderfetalgenetic approachgenetic strategygerm free conditionglobal gene expressionglobal transcription profileidiopathic steatorrheaimprintinflammatory disease of the intestineinflammatory disorder of the intestineinsightintestinal autoinflammationintestinal pathogenintestine pathogenkiller T cellliability to diseaselymph cellmalignancymicrobialmicrobial consortiamicrobial floramicrobiotamicrofloramouse modelmultispecies consortiamurine modelnatural killer T lymphocyteneoplasm/cancernovelpathogenpathwaypharmacologicpreventpreventingresistantscRNA sequencingscRNA-seqsingle cell RNA-seqsingle cell RNAseqsingle cell expression profilingsingle cell transcriptomic profilingsingle-cell RNA sequencingsmall bowelsocial rolespecific pathogen freetranscriptome
Description preview
PROJECT SUMMARY/ABSTRACT
CD1d-restricted, invariant natural killer T cells (iNKT) cells play a critical role in regulating the commensal micro-
biota and resistance to mucosal pathogens. Conversely, iNKT cell levels are suppressed by microbiota in early
(pre-weaned), but not later (post-weaned), life. If critical microbial signals are not provided…
🔒
Start 7-day free trial — $29.99/mo →Full details available on the Agency plan
Unlock the complete grant description, eligibility criteria, contract value, evaluation details and apply link — plus alerts, pipeline tracking, and CSV export.
Agency Plan
7-day free trialUnlock procurement & grants
Upgrade to access active tenders from World Bank, UNDP, ADB and more — with email alerts and pipeline tracking.
$29.99 / month
- 🔔Email alerts for new matching tenders
- 🗂️Track tenders in your pipeline
- 💰Filter by contract value
- 📥Export results to CSV
- 📌Save searches with one click