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Molecular regulation of T cell activation signals by TRAF3

TRAF3 对 T 细胞激活信号的分子调节

基本信息

批准号：
9211288
负责人：
GAIL A. BISHOP
金额：
$ 38.13万
依托单位：
UNIVERSITY OF IOWA
依托单位国家：
美国
项目类别：
财政年份：
2016
资助国家：
美国
起止时间：
2016-02-01 至 2021-01-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9211288
关键词：
Adaptor Signaling Protein Address Antigen Receptors Autoimmune Process B-Lymphocytes Behavior Biological Response Modifiers CD28 gene CD3 Antigens Cell Line Cells Cellular biology Communicable Diseases Complex Cytokine Receptors Cytoplasm Cytoplasmic Tail Data Effector Cell Epithelial Family Fibroblasts Health IFNAR1 gene Immune Immune checkpoint inhibitor Immune system Immunology Inflammatory Interferon Receptor Knowledge Lead Ligation Lymphocyte Biology Mediating Membrane Mission Mitogen-Activated Protein Kinases Molecular Myelogenous Myeloid Cells Nature Organism Outcome PTPN22 gene Pathway interactions Phosphoric Monoester Hydrolases Phosphotransferases Play Process Proteins Public Health Publishing Receptor Cell Receptor Signaling Recruitment Activity Regulation Research Role Signal Pathway Signal Transduction T cell regulation T-Cell Activation T-Cell Receptor T-Lymphocyte TNF Receptor-Associated Factors TNF receptor-associated factor 3 TNFRSF5 gene Therapeutic Tumor Necrosis Factor Receptor United States National Institutes of Health cell type cytokine improved member novel overexpression protein protein interaction public health relevance receptor tumor type I interferon receptor

项目摘要

DESCRIPTION (provided by applicant): The number and variety of immune cell receptors and signaling pathways shown to be regulated by the tumor necrosis factor receptor (TNFR)-associated factors (TRAFs) has steadily grown in recent years. TRAF3, initially identified through its association with the CD40 receptor, has emerged as an especially versatile regulator of immune processes. Previously, TRAF3 was studied primarily in B lymphocytes, myeloid cells, and non-immune cells. However, recent studies reveal that TRAF3 also plays several important and distinct roles in regulation of T lymphocyte biology, although how this occurs is only starting to be unraveled. The proposed project focuses upon this knowledge gap, and aims to fulfill a critical need to understand how TRAF3 regulates T cell activation. This question will be pursued in three Specific Aims, to uncover: 1) The role of TRAF3 in facilitating TCR signaling. 2) The role of TRAF3-CD28 interactions in regulation of T cell signaling and 3) The role of TRAF3 in restraining signaling to T cells by the type 1 interferon receptor (IFNAR). The expected outcomes of this project are important new knowledge that will revise fundamental understanding of T cell signaling, providing novel basic immunology knowledge that will in turn inform potential therapeutic applications that seek to manipulate the process of T cell activation.