Regulation of LAIR-1 in Lupus

LAIR-1 在狼疮中的调节

• 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
• 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

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）：系统性红斑狼疮（SLE）是一种自身免疫性疾病，有遗传和非遗传触发。已知C1 q缺乏易患SLE，表明C1 q有助于维持耐受性。研究表明，C1 q触发白细胞相关的Ig样受体-1（LAIR-1）的激活，为理解C1 q介导的耐受机制提供了一些合理的线索。我们最近的研究表明丁酸盐上调LAIR-1的表达。本研究的目的是了解LAIR-1是如何调节的，以及它如何与C1 q一起有助于疾病预防。这些研究可能有助于确定SLE的潜在治疗靶点。因此，我们建议：了解C1 q介导的LAIR-1激活机制。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。通过对这三个相关问题的研究，我们将进一步阐明SLE发病机制的新的生物学和临床见解。