Cell/Tissue Damage and Autoimmune Response

描述(申请人提供)：虽然自身免疫性疾病的遗传本质已经被很好地确定，但遗传相关的自身免疫性疾病的易感性转化为特定疾病启动的具体机制充其量还知之甚少。随着对自身免疫性疾病启动机制的更好理解，可以启动研究和开发计划，以开发自身免疫疗法。在座谈会上要讨论的中心问题是细胞/组织损伤和自身免疫反应。关注细胞损伤作为自身免疫性疾病的始发者的作用。这次座谈会的目标是确定在这一领域进行关键研究的机会，这些机会代表着未得到满足的需求或目前资金不足。这将是一次新奇的座谈会。旨在将具有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呈现一组谈话。研讨会将采用多学科的方法来实现这一目标：通过将来自广泛学科的专家聚集在一起，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，我们打算挑战和扩展我们对自身免疫性疾病的思考方式。周五的总体计划是以两个截然不同、有争议的演讲开始，主题是细胞损伤是自身免疫性疾病的原因还是贡献者。周六，将有四个会议都围绕同一个核心问题：是什么导致了自身免疫性疾病？25位发言者将被要求就自身免疫性疾病的原因作一次简短的演讲，并参考我的工作。随后将与职业讨论者领袖进行一般性讨论。周日将专门举行分组会议、总结报告和确定未得到满足的研究需求。该节目将由包括诺埃尔·罗斯、贝蒂·戴蒙德和埃里克·格什温在内的著名研究人员发表演讲。分组会议将由主席和讨论领导人推动，目的是促进资深和年轻研究人员之间的相互交谈和公开讨论。总体而言，我们预计有25到30名演讲者和大约75到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。

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.