Transcriptional Regulation of Innate T cell fate

先天 T 细胞命运的转录调控

基本信息

  • 批准号:
    10283893
  • 负责人:
  • 金额:
    $ 23.33万
  • 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
  • 起止时间:
    2021-07-14 至 2023-06-30
  • 项目状态:
    已结题

项目摘要

Project Summary InnateT cells are a collection of T cells withimportant regulatory functions that have a crucial role in immunity towards tumors, bacteria, viruses, and in cell-mediated autoimmunity. Due large quantities of cytokines upon activation, immune response populations glycolipid cells T commitment to innate T cells act as bridges between the innate and adaptive systems a nd ontribute greatly In mice, this swiftness of reflects their acquisition f functionality during their development in the thymus. Three major within the innate T cell group are recognized namely, the invariant NKT cells that recognize antigens presented by non-polymorphic CD1d molecules, the mucosal associated invariant T (MAIT) that recognize vitamin metabolites presented by the non-polymorphic MR1 molecules, and the certain  cells which antigen specificities remain uncertain. We have established an in vitro system t hat mimics the of double positive precursor cells to the innate T cell lineage and we propose to their ability to promptly secrete c to immune regulation and host protection. o , deconstruct the early transcriptional and epigenetic events that accompany this fate commitment (Aim 1). In this way, we will identify manipulation early factors that influence innate T cell development, providing the possibility for selective of innate T cell lineage specification. We will then investigatewhether human innate T cells acquire an innate-like transcriptional program in the thymus similarly to their mouse counterparts and whether this program is shared between the two species. To do so, we will profile the transcriptomes of iNKT and MAIT cells purified from neonatal human thymi at the single cell level. In addition, we will extend our knowledge of innate T cell lineage commitment by also studying CD1a-restricted T cells, which do not exist in mice (Aim 2). Given their capacity to link key inflammatory axes of innate and adaptive immunity, a better understanding of the molecular basis underpinning innate T cell development and plasticity, and how much this feature accounts for their pathophysiological roles, is critical for developing novel therapeutic approaches.
项目总结

项目成果

期刊论文数量(0)
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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Laurent Gapin其他文献

Laurent Gapin的其他文献

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{{ truncateString('Laurent Gapin', 18)}}的其他基金

Transcriptional Regulation of Innate T cell fate
先天 T 细胞命运的转录调控
  • 批准号:
    10450153
  • 财政年份:
    2021
  • 资助金额:
    $ 23.33万
  • 项目类别:
Genetic determinants of "innate" T lymphocytes development and homeostasis
“先天”T 淋巴细胞发育和稳态的遗传决定因素
  • 批准号:
    10412121
  • 财政年份:
    2021
  • 资助金额:
    $ 23.33万
  • 项目类别:
Role of MAIT cells in a mouse model of spontaneous colitis
MAIT细胞在自发性结肠炎小鼠模型中的作用
  • 批准号:
    10436375
  • 财政年份:
    2021
  • 资助金额:
    $ 23.33万
  • 项目类别:
Role of MAIT cells in a mouse model of spontaneous colitis
MAIT细胞在自发性结肠炎小鼠模型中的作用
  • 批准号:
    10300940
  • 财政年份:
    2021
  • 资助金额:
    $ 23.33万
  • 项目类别:
Genetic determinants of "innate" T lymphocytes development and homeostasis
“先天”T 淋巴细胞发育和稳态的遗传决定因素
  • 批准号:
    10251641
  • 财政年份:
    2021
  • 资助金额:
    $ 23.33万
  • 项目类别:
TCR signal strength and iNKT cell subset development
TCR 信号强度和 iNKT 细胞亚群发育
  • 批准号:
    10447807
  • 财政年份:
    2018
  • 资助金额:
    $ 23.33万
  • 项目类别:
TCR signal strength and iNKT cell subset development
TCR 信号强度和 iNKT 细胞亚群发育
  • 批准号:
    9981614
  • 财政年份:
    2018
  • 资助金额:
    $ 23.33万
  • 项目类别:
TCR signal strength and iNKT cell subset development
TCR 信号强度和 iNKT 细胞亚群发育
  • 批准号:
    9761964
  • 财政年份:
    2018
  • 资助金额:
    $ 23.33万
  • 项目类别:
TCR signal strength and iNKT cell subset development
TCR 信号强度和 iNKT 细胞亚群发育
  • 批准号:
    10219060
  • 财政年份:
    2018
  • 资助金额:
    $ 23.33万
  • 项目类别:
Role of mCD1D2 in iNKT cell development and functions
mCD1D2 在 iNKT 细胞发育和功能中的作用
  • 批准号:
    9431944
  • 财政年份:
    2018
  • 资助金额:
    $ 23.33万
  • 项目类别:

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