Lung leukocytes promote alveolar epithelial regeneration after severe injury
肺白细胞促进严重损伤后肺泡上皮再生
基本信息
- 批准号:10666350
- 负责人:
- 金额:$ 62.04万
- 依托单位:
- 依托单位国家:美国
- 项目类别:
- 财政年份:2020
- 资助国家:美国
- 起止时间:2020-05-01 至 2025-04-30
- 项目状态:未结题
- 来源:
- 关键词:AblationAcuteAcute Lung InjuryAlveolarAmphiregulinAnatomyBindingCellsChronicCuesDevelopmentDisease modelDistalEnvironmentEpidermal Growth Factor ReceptorEpithelial CellsEpitheliumExhibitsFunctional disorderFutureGene ExpressionGeneticGoalsGrowth FactorHomeostasisImageImmuneImmune responseImmune signalingImmune systemImpairmentInfectionInflammationInflammation MediatorsInflammatoryInjuryKineticsLeucocytic infiltrateLeukocytesLigandsLinkLungLung diseasesLymphocyteMediatingMesenchymalMesenchymal Stem CellsMetabolicModelingMolecularMusNatural regenerationOrganOutcomePathogenicityPatternPhasePhysiologicalPlayPopulationProcessProductionProliferatingRegenerative MedicineRegulationRegulatory T-LymphocyteReport (document)ResolutionRoleSeveritiesSignal InductionSignal TransductionSourceSpatial DistributionSterilityStimulusStructure of parenchyma of lungSupporting CellT-LymphocyteTestingTissuesTumor ImmunityViral Respiratory Tract InfectionWound modelsairway regenerationalveolar epitheliumcell typeepithelial stem cellepithelium regenerationimmunological diversityin vivoinfluenza infectioninfluenzavirusinterdisciplinary approachlung injurylung preservationlung regenerationlung repairorgan growthpathogenprogenitorprogramsprotective factorspulmonary functionrecruitregenerativerepairedresponserestorationsevere injuryskin woundstemstem cell populationstem cellstherapeutic candidatetherapeutic developmenttissue injurytissue regenerationtissue repairtool
项目摘要
PROJECT SUMMARY/ABSTRACT
It has become increasingly appreciated that lymphocytes within non-lymphoid tissues exhibit unique effector
programs that extend beyond their roles in anti-pathogen and anti-tumor immunity. Such non-immune functions,
including the regulation of metabolic homeostasis and tissue repair, highlight the diversity of immunological
signals that can be elaborated in a tissue-specific manner to modify physiological and developmental parameters
within a given niche. To achieve these diverse regulatory roles, tissue-localized leukocytes interact with
specialized non-lymphoid cells that define the organ’s function, triggering niche-specific effector programs in
response to perturbations within the tissue microenvironment. In support of this mechanism, a recently described
population of lung regulatory T (Treg) cells were shown to play a pronounced tissue-protective role during the
early stages of acute lung injury caused by influenza virus infection in mice. Through their production of the
epidermal growth factor receptor (EGFR) ligand, amphiregulin, these Treg cells support epithelial barrier
regeneration and preserve lung function. Although these findings uncovered an important and previously
unknown role for Treg cell–derived amphiregulin, the mechanistic details of how amphiregulin influences lung
repair remained undetermined. Preliminary studies indicate that in response to lung injury caused by other
damaging stimuli, infiltrating leukocyte populations other than regulatory T cells produce amphiregulin. Further
inspection has suggested that amphiregulin-producing leukocytes may guide alveolar epithelial regeneration by
interacting with specific lung mesenchymal and epithelial stem/progenitor cell populations that orchestrate
discrete steps of the repair process. To this end, the major goals of this proposal are to 1) characterize
interactions between amphiregulin-producing lung leukocytes and resident mesenchymal and epithelial
stem/progenitor cells, 2) identify the molecular basis of these interactions and define their relative significance
for restoring normal lung function, and 3) determine how these cellular interactions are influenced by the severity
or type of damaging stimuli. Successful completion of this project will broaden our understanding of the role of
tissue-specific immune responses in directing tissue regeneration and support the development of future
strategies that seek to stimulate these processes to treat lung disease and restore normal organ homeostasis.
项目总结/文摘
项目成果
期刊论文数量(1)
专著数量(0)
科研奖励数量(0)
会议论文数量(0)
专利数量(0)
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Nicholas Arpaia其他文献
Nicholas Arpaia的其他文献
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Lung leukocytes promote alveolar epithelial regeneration after severe injury
肺白细胞促进严重损伤后肺泡上皮再生
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$ 62.04万 - 项目类别:
Lung leukocytes promote alveolar epithelial regeneration after severe injury
肺白细胞促进严重损伤后肺泡上皮再生
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10225703 - 财政年份:2020
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$ 62.04万 - 项目类别:
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