Cell/Tissue Damage and Autoimmune Response

细胞/组织损伤和自身免疫反应

• 批准号: 7163575
• 负责人: Noel R. Rose
• 金额: $ 4.5万
• 依托单位: AMERICAN AUTOIMMUNE RELATED DIS ASSOC
• 依托单位国家: 美国
• 财政年份: 2006
• 资助国家: 美国
• 起止时间: 2006-06-20 至 2007-05-31
• 项目状态: 已结题
• 来源: https://reporter.nih.gov/project-details/7163575
• 关键词: autoimmune disorder; autoimmunity; cellular pathology; cytotoxicity; disease /disorder etiology; genetic susceptibility; meeting /conference /symposium; pathologic process; travel

DESCRIPTION (provided by applicant): Although the hereditary nature of autoimmune disease has been well established, the specific mechanisms by which hereditary-related susceptibility to autoimmune disease translates to specific disease initiation are poorly understood at best. With a better understanding of the mechanisms surrounding autoimmune disease initiation, research and development programs could be initiated toward the development of autoimmune therapies. The central question to be addressed at the colloquium, .Cell/Tissue Damage and Autoimmune Response. concerns the role of cell injury as an initiator of autoimmune disease. The goal of this colloquium is to identify opportunities for critical research in this area that represent unmet needs or are currently underfunded. This will be a novel colloquium (i.e. .talking among.) designed to bring together investigators of diverse backgrounds and interests for discussion and conversation, rather than simply presenting a set talk with familiar data. The colloquium will adopt a multidisciplinary approach in meeting this objective: By bringing together specialists from a wide range of disciplines, including but not limited to microbiologists, geneticists, infectious disease specialists, cellular biologists, environmentalists, immunologists, molecular biologist, etc., we intend to challenge and extend the way we think about autoimmune diseases. The overall plan is to start Friday with two contrasting, controversial talks in the general theme of cell injury as a cause or contributor to autoimmune disease. On Saturday, there would be four sessions all on the same core question: What causes autoimmune disease? Each of the twenty-five speakers would be asked to give a short talk on the cause of autoimmune disease with reference to my work. This would be followed by general discussion with provacateur discussant leader. Sunday would be devoted to a break-out session, summary reports and identification of unmet research needs. The program will feature presentations by eminent researchers including Noel Rose, Betty Diamond and Eric Gershwin. The break-out sessions will be facilitated by the chairpersons and discussion leaders with an aim toward stimulating cross-talk and open discussions between both veteran and young researchers. Overall, we anticipate a faculty of 25 to 30 speakers, and about 75 to 100 attendees. After the colloquium, our ultimate goal is to publish the meeting report in a well-circulated journal.

描述（由申请人提供）：尽管自身免疫性疾病的遗传性质已得到充分确立，但与遗传性相关的自身免疫性疾病的敏感性转化为特定的特定疾病起始的特定机制，充其量是对特定的。有了更好地了解围绕自身免疫性疾病启动的机制，可以启动研发计划，以开发自身免疫疗法。在座谈会，细胞/组织损伤和自身免疫反应时要解决的中心问题。涉及细胞损伤作为自身免疫性疾病的发起者的作用。该座谈会的目的是在该领域确定代表未满足需求或目前资助不足的重要研究机会。 这将是一种新颖的座谈会（即。座谈会将采用多学科的方法来满足这一目标：通过将各种学科的专家汇集在一起​​，包括但不限于微生物学家，遗传学家，传染病专家，细胞生物学家，环保主义者，免疫学家，分子生物学家等。总体计划是在周五开始，以两次对比的，有争议的对话，是细胞损伤的一般主题，是自身免疫性疾病的原因或贡献者。在星期六，在同一核心问题上会有四个会议：是什么导致自身免疫性疾病？二十五名演讲者中的每一个都会被要求就我的工作进行简短的关于自身免疫性疾病的事业的讨论。随后将与Peracateur讨论者负责人进行一般讨论。周日将致力于分手会议，摘要报告和确定未满足的研究需求。该计划将展示包括Noel Rose，Betty Diamond和Eric Gershwin在内的著名研究人员的演讲。主席和讨论领袖将促进分手会议，以刺激老兵与年轻研究人员之间的串扰和公开讨论。总体而言，我们预计将有25至30名演讲者，约75至100名与会者。座谈会之后，我们的最终目标是在一本通畅的日记中发布会议报告。