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Mechanisms of E protein transcription factor-dependent iNKT cell expansion and differentiation

E蛋白转录因子依赖性iNKT细胞扩增和分化的机制

基本信息

批准号：
9242168
负责人：
BARBARA L. KEE
金额：
$ 39.69万
依托单位：
UNIVERSITY OF CHICAGO
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：
2016-12-19 至 2021-11-30
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9242168
关键词：
Alpha Cell Antigens Applications Grants Asthma Atherosclerosis Autoimmune Diseases Autoimmunity BCL6 gene CD4 Positive T Lymphocytes CD8-Positive T-Lymphocytes CD8B1 gene Cell Count Cell Differentiation process Cell Lineage Cell physiology Cells Cytotoxic T-Lymphocytes Data Dendritic Cells Development Disease E protein Ectopic Expression Effector Cell Ensure Failure GATA3 gene Gene Expression Gene Expression Profile Gene Targeting Genetic Transcription Glycolipids Grant Hypersensitivity ID2 gene IL17 gene IL4 gene IgE Immune Immune response Immune system Insulin-Dependent Diabetes Mellitus Intercept Interferon Type II Interleukin-7 Invaded Malignant Neoplasms Memory Molecular Multiple Sclerosis Mus Natural Immunity Phenotype Play Population Predisposition Production Proteins Regulation Repression Research Rheumatoid Arthritis Role Serum Specific qualifier value System Systemic Lupus Erythematosus T-Cell Receptor T-Lymphocyte T-Lymphocyte Subsets TCF3 gene Testing Therapeutic Therapeutic Agents Thymus Gland Tuberculosis WNT Signaling Pathway ZNF145 gene adaptive immunity antimicrobial base c-myc Proto-Oncogenes cell type cytokine experimental study graft vs host disease helix-loop-helix protein differentiation inhibitor in vivo in vivo Model inhibitor/antagonist insight mutant novel pathogen protein E thymocyte transcription factor

项目摘要

Project Summary Invariant natural killer T (iNKT) cells are a subset of T lymphocytes that sit at the boarder of adaptive and innate immunity. They have highly restricted T cell receptors (TCRs) that detect glycolipid antigen presented by the non-classical MHC molecule CD1d and they respond rapidly to antigen or cytokine stimulation. NKT cells play an important role in anti-microbial immune responses and because of their rapid production of multiple cytokines they are being considered as therapeutic agents in cancer and other diseases. NKT cells acquire their effector phenotype as a consequence of their unique mechanism of selection and differentiation in the thymus. The range of effector fates that NKT cells can acquire is only beginning to be appreciated but the mechanisms controlling NKT cell effector fate choice are completely unknown. Our research is directed at understanding the molecular mechanisms that control iNKT cell development with a focus on the E protein transcription factors, their inhibitors the ID proteins, and their downstream targets. These proteins are critical regulators of iNKT cell numbers and effector cell fate choice. In this grant application we propose experiments to determine the requirements for E2A in iNKT cell development an the consequences of over- and under-expression of two putative E2A target genes, Lef1 and Bcl6. Our studies will have a major impact on our understanding of how NKT cell number and function is regulated. In addition, our studies will provide insight into mechanisms to manipulate NKT cell effector fate and thereby alter immune responses at their inception.

项目总结