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证实，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具体机制充其量仍知之甚少。随着对自身免疫性疾病发生机制的更好了解，可以启动研究和开发计划以开发自身免疫疗法。研讨会要解决的核心问题是细胞/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引发剂的作用。本次研讨会的目标是确定该领域未满足需求或目前资金不足的关键研究机会。 这将是一个新颖的座谈会（即相互交谈），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固定的谈话。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，我们旨在挑战和扩展我们对自身免疫性疾病的思考方式。总体计划是从周五开始，以细胞损伤作为自身免疫性疾病的原因或促成因素为主题，进行两场截然不同的、有争议的演讲。周六，将有四场会议讨论同一核心问题：自身免疫性疾病的原因是什么？二十五位演讲者中的每一位都会被要求结合我的工作就自身免疫性疾病的原因进行简短的演讲。随后将与煽动者讨论领袖进行一般性讨论。周日将专门举行分组会议、总结报告和确定未满足的研究需求。该节目将由诺埃尔·罗斯 (Noel Rose)、贝蒂·戴蒙德 (Betty Diamond) 和埃里克·格什温 (Eric Gershwin) 等著名研究人员进行演讲。分组会议将由主席和讨论负责人主持，旨在激发资深研究人员和年轻研究人员之间的交叉对话和公开讨论。总体而言，我们预计将有 25 至 30 名演讲者和大约 75 至 100 名与会者。研讨会结束后，我们的最终目标是在一份广为流传的期刊上发表会议报告。