Administrative Core

行政核心

• 批准号: 8733827
• 负责人: CORNELIS P TERHORST
• 金额: $ 6.63万
• 依托单位: BETH ISRAEL DEACONESS MEDICAL CENTER
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-08-15 至
• 项目状态: 未结题
• 来源: https://reporter.nih.gov/project-details/8733827
• 关键词: Autoimmunity; Biological Markers; Cell Communication; Cells; Chromatin; Complement; Diagnostic; Disease; Gene Family; Genetic; Goals; Human; Immune; Lead; Ligands; Lupus; Monitor; Mus; Outcome; Pathogenesis; Pathway interactions; Patients; Pharmaceutical Preparations; Predisposition; Reagent; Research Personnel; Role; SLAM family receptor; Signal Transduction; System; Systemic Lupus Erythematosus; Therapeutic; To autoantigen; Translational Research; Treatment Protocols; base; indexing; insight; meetings; member; novel; programs; receptor; research study; tool

This application seeks support for elucidating the role of the SLAMF receptors in the pathogenesis of Systemic Lupus Erythematosus (SLE) with the ultimate goal to develop SLAMF-based therapeutic strategies that can be applied to SLE patients. Because of the outcomes of our studies with cells derived from SLE patients and our exciting findings with genetically altered mice, which develop lupus-related autoimmunity, we now have the systems in place to dissect how cell interaction mechanisms and signaling initiated by the SLAMF receptors contribute to the control of tolerance to autoantigens and to the pathogenesis of human SLE. These insights and tools are the basis for a Program Project application entitled: "SLAM FAMILY RECEPTOR CONTROLLED PATHWAYS TO SLE" for three interlinked projects and two supporting Cores. P#1 The Slamf3, Slamf5 and Slamf6 receptor-induced pathways to murine lupus. P#2 Functional analyses of human and mouse SLAMF4«SLAMF2 receptor / ligand interactions in murine and human SLE. P#3 Function of human SLAMF receptors in SLE immune cells. PL: Core A Genetic Mouse Core. Core B Administrative Core. In this Administrative Core we specifically propose to: SA#1. Nurture scientific interactions between the investigators in the three projects in the program through frequent meetings; particularly by streamlining the transition from mouse experiments to Translational Research with materials from SLE patients. SA#2. Facilitate the exchange of reagents, technical information and patient materials. SA#3. Facilitate administrative interactions between the members of the program.

本申请寻求对阐明SLAMF受体在肿瘤发病机制中的作用的支持。 系统性红斑狼疮（SLE），最终目标是开发基于SLAMF的治疗策略 可以应用于SLE患者。由于我们对SLE细胞的研究结果， 病人和我们令人兴奋的发现与转基因小鼠，其中发展狼疮相关的自身免疫， 我们现在已经有了系统来剖析细胞相互作用机制和信号是如何由细胞内的 SLAMF受体有助于控制对自身抗原的耐受性和人类免疫性疾病的发病机制。 SLE。 这些见解和工具是一个名为“SLAM家族”的计划项目应用程序的基础 三个相互关联的项目和两个支持核心的“接收方控制的SLE途径”。 P#1 Slamf 3、Slamf 5和Slamf 6受体诱导的小鼠狼疮途径。 P#2在小鼠中人和小鼠SLAMF 4·SLAMF 2受体/配体相互作用的功能分析 和人SLE。 P#3 SLE免疫细胞中人SLAMF受体的功能。预许可： 核心基因小鼠核心。 核心B管理核心。 在本行政核心中，我们特别建议： SA #1。通过以下方式培养项目中三个项目的研究人员之间的科学互动 频繁的会议;特别是通过简化从小鼠实验到转化实验的过渡 SLE患者材料的研究。 SA #2。促进试剂、技术信息和患者材料的交流。 SA #3。促进项目成员之间的管理互动。