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Developing tools to study relationship between oxidative stress in T cell dysfunction

开发工具来研究 T 细胞功能障碍中氧化应激之间的关系

基本信息

批准号：
10516748
负责人：
Takeshi Egawa
金额：
$ 7.85万
依托单位：
WASHINGTON UNIVERSITY
依托单位国家：
美国
项目类别：
财政年份：
2021
资助国家：
美国
起止时间：
2021-11-01 至 2023-10-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/10516748
关键词：
3&apos Untranslated Regions Affinity Chromatography Alleles Antibodies Antigens Automobile Driving BLR1 gene CD8-Positive T-Lymphocytes Cell Cycle Arrest Cells Cellular Stress Chronic Classification Clinic DNA Damage Data Detection Enterobacteria phage P1 Cre recombinase Exhibits Exposure to Functional disorder Future Gene Expression Gene Expression Profiling Genes Goals Grant Immune response Immunohistochemistry Immunotherapy Impairment In Situ In Vitro Infection Infection Control Knock-in Knock-in Mouse Literature Lymphocytic choriomeningitis virus Malignant Neoplasms Manuscripts Mus Neoplasm Transplantation Oryctolagus cuniculus Oxidative Stress Oxidative Stress Induction Oxidative Stress Pathway PD-1 blockade Phenotype Play Population Pre-Clinical Model Process Proliferating Proteomics Publishing Reporter Residual state Role Stains Surface T-Lymphocyte Therapeutic Treatment Efficacy Virus Diseases Visualization biological adaptation to stress cell type conditional knockout effector T cell exhaust exhaustion experimental study gene product improved in vivo pathogen polyclonal antibody progenitor programmed cell death protein 1 programs receptor response segregation single-cell RNA sequencing stem tool transcription factor transplant model tumor tumor growth tumor microenvironment

项目摘要

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.

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。