Developing tools to study relationship between oxidative stress in T cell dysfunction
Developing tools to study relationship between oxidative stress in T cell dysfunction
批准号:
10516748
负责人:
Takeshi Egawa
金额:
$7.85万
依托单位:
依托单位国家:
美国
项目类别:
财政年份:
2021
资助国家:
美国
项目状态:
已结题
起止时间:
2021-11-01 至 2023-10-31
关键词:
3&apos Untranslated RegionsAffinity ChromatographyAllelesAntibodiesAntigensAutomobile DrivingBLR1 geneCD8-Positive T-LymphocytesCell Cycle ArrestCellsCellular StressChronicClassificationClinicDNA DamageDataDetectionEnterobacteria phage P1 Cre recombinaseExhibitsExposure toFunctional disorderFutureGene ExpressionGene Expression ProfilingGenesGoalsGrantImmune responseImmunohistochemistryImmunotherapyImpairmentIn SituIn VitroInfectionInfection ControlKnock-inKnock-in MouseLiteratureLymphocytic choriomeningitis virusMalignant NeoplasmsManuscriptsMusNeoplasm TransplantationOryctolagus cuniculusOxidative StressOxidative Stress InductionOxidative Stress PathwayPD-1 blockadePhenotypePlayPopulationPre-Clinical ModelProcessProliferatingProteomicsPublishingReporterResidual stateRoleStainsSurfaceT-LymphocyteTherapeuticTreatment EfficacyVirus DiseasesVisualizationbiological adaptation to stresscell typeconditional knockouteffector T cellexhaustexhaustionexperimental studygene productimprovedin vivopathogenpolyclonal antibodyprogenitorprogrammed cell death protein 1programsreceptorresponsesegregationsingle-cell RNA sequencingstemtooltranscription factortransplant modeltumortumor growthtumor microenvironment
中文摘要
摘要
在慢性病毒感染或肿瘤微环境中,抗原(Ag)特异性CD8 T细胞
经历交替的激活过程,称为耗尽。耗尽的CD8 T细胞失去其增殖,
效应基因表达,从而允许病毒感染或肿瘤生长持续,尽管最初的扩张,
抗原特异性克隆。虽然驱动T细胞耗竭的确切机制是未知的,但文献
表明T细胞暴露于过度的氧化应激有助于疲劳的建立。
在这一小笔赠款中,我们建议生产转基因小鼠,以促进细胞的可视化,
暴露于氧化应激,并使用工具进行T细胞耗竭的未来研究。
英文摘要
Abstract
In response to chronic viral infection or in tumor microenvironment, antigen(Ag)-specific CD8 T cells
undergo alternative activation processes, called exhaustion. Exhausted CD8 T cells lose their proliferation and
effector gene expression, thus allowing viral infection or tumor growth to persist despite the initial expansion of
antigen-specific clones. Although the precise mechanism driving T cell exhaustion is unknown, literature
suggests that exposure of T cells to excessive oxidative stress contribution to the establishment of exhaustion.
In this small grant, we propose to generate genetically modified mice that facilitate visualization of cells that are
exposed to oxidative stress and use the tools for future studies for T cell exhaustion.
期刊论文(0)
专著(0)
科研奖励(0)
会议论文
CD8 T cell fate decision instructed by IL-2
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Developing tools to study relationship between oxidative stress in T cell dysfunction
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批准号:10362128
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Regulation of Normal and Pathogenic B Cell Proliferation by a c-Myc-initiated Transcription Factor Cascade
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Regulation of Normal and Pathogenic B Cell Proliferation by a c-Myc-initiated Transcription Factor Cascade
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Regulation of Normal and Pathogenic B Cell Proliferation by a c-Myc-initiated Transcription Factor Cascade
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The transcription factor c-MYC in lymphocyte expansion and restriction of stemness
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REGULATION OF LYMPHOCYTE METABOLISM AND HOMEOSTATIS BY THE C-MYC/AP4 AXIS
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财政年份:2015
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GENE REGULATION GOVERNING T LYMPHOCYTE FATE DECISIONS
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资助金额:$38.0万
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财政年份:2012
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GENE REGULATION GOVERNING T LYMPHOCYTE FATE DECISIONS
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财政年份:2012
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依托单位:
GENE REGULATION GOVERNING T LYMPHOCYTE FATE DECISIONS
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批准号:8707185
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资助金额:$38.0万
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财政年份:2012
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负责人:Takeshi Egawa
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依托单位:
海外基金