Regulation of LAIR-1 in Lupus

LAIR-1 在狼疮中的调节

基本信息

批准号：
9120806
负责人：
Myoungsun Son
金额：
$ 12.77万
依托单位：
FEINSTEIN INSTITUTE FOR MEDICAL RESEARCH
依托单位国家：
美国
项目类别：
财政年份：
2014
资助国家：
美国
起止时间：
2014-09-16 至 2019-08-31
项目状态：
已结题

来源：
https://reporter.nih.gov/project-details/9120806
关键词：
Address Antibodies Autoimmune Diseases Autoimmunity B-Lymphocytes Binding Sites Biological Butyrates Cells Clinical Complement Complement 1q Consensus Defect Dendritic Cells Disease Epigenetic Process Exhibits Genetic Goals Health Histone Deacetylase Inhibitor Human Immune Immune Tolerance In Vitro Inflammation Interferon-alpha Interleukin-10 Interleukin-4 Interleukin-6 Lead Learning Leukocytes Link Lupus Mediating Modeling Modification Mus Outcome Pathogenesis Pathway interactions Patients Pattern Phenotype Production Regulation Research Personnel Risk Factors Severities Signal Transduction Systemic Lupus Erythematosus TNF gene Testing Therapeutic Transcription Coactivator adaptive immunity career chronic autoimmune disease complement 1q receptor cytokine disorder prevention experience in vivo inhibitor/antagonist insight lupus-like member monocyte new technology new therapeutic target non-genetic prevent promoter receptor therapeutic target

项目摘要

DESCRIPTION (provided by applicant): Systemic lupus erythematosus (SLE) is an autoimmune disease that has both genetic and nongenetic triggers. C1q deficiency is known to predispose to SLE, demonstrating that C1q helps maintain tolerance. Studies showing that C1q triggers leukocyte-associated Ig-like receptor-1 (LAIR-1) activation have yielded some reasonable clues for understanding tolerance mechanisms mediated by C1q. Our recent studies have revealed that butyrate up-regulates the expression of LAIR-1. The goal of this study is to understand how LAIR-1 is regulated and how it, together with C1q, contributes to disease prevention. These studies may help identify potential therapeutic targets in SLE. We therefore propose to: 1. Understand the mechanism of C1q-mediated LAIR-1 activation. 2. Understand factors regulating expression of LAIR-1. 3. Test the contribution of LAIR-1 to lupus models. By studying three relevant questions, we will further define new biological and clinical insights of SLE pathogenesis.

描述（由申请人提供）：全身性红斑狼疮（SLE）是一种自身免疫性疾病，既有遗传和非遗传触发器。已知C1Q缺乏症会易于SLE，这表明C1Q有助于保持耐受性。研究表明，C1Q触发白细胞相关的Ig样受体1（LAIR-1）激活产生了一些合理的线索，以理解由C1Q介导的耐受性机制。我们最近的研究表明，丁酸酯上调了LAIR-1的表达。这项研究的目的是了解Lair-1的调节方式，以及它如何与C1Q一起有助于预防疾病。这些研究可能有助于确定SLE中潜在的治疗靶标。因此，我们建议：1。了解C1Q介导的LAIR-1激活的机理。 2。了解调节Lair-1表达的因素。 3。测试Lair-1对狼疮模型的贡献。通过研究三个相关问题，我们将进一步定义SLE发病机理的新生物学和临床见解。