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经得到很好的确定，但对自身免疫性疾病的遗传相关易感性转化为特定疾病起始的特定机制知之甚少。随着对自身免疫性疾病启动机制的更好理解，可以启动针对自身免疫性疗法开发的研究和开发计划。在学术讨论会上要解决的中心问题，细胞/组织损伤和自身免疫反应。涉及细胞损伤作为自身免疫性疾病的引发剂的作用。本次座谈会的目标是确定在这一领域开展关键研究的机会，这些研究代表着未满足的需求或目前资金不足。 这将是一个新的座谈会（即。旨在将不同背景和兴趣的研究人员聚集在一起进行讨论和对话，而不是简单地用熟悉的数据进行一系列谈话。研讨会将采用多学科方法来实现这一目标：通过汇集来自广泛学科的专家，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，环境学家，免疫学家，分子生物学家等，我们打算挑战和扩展我们对自身免疫性疾病的看法。总体计划是从星期五开始，在细胞损伤作为自身免疫性疾病的原因或贡献者的总主题上进行两次对比鲜明、有争议的会谈。星期六，将有四个会议都在同一个核心问题：是什么导致自身免疫性疾病？25位演讲者中的每一位都将被要求就自身免疫性疾病的原因做一个简短的演讲，参考我的工作。随后将与省长讨论人领导人进行一般性讨论。星期天将专门举行分组会议，总结报告和确定未满足的研究需求。该计划将由著名的研究人员，包括诺埃尔罗斯，贝蒂钻石和埃里克格什温介绍。分组会议将由主席和讨论领导人主持，目的是激发资深和年轻研究人员之间的交流和公开讨论。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。座谈会结束后，我们的最终目标是在一份发行量很大的期刊上发表会议报告。