Conference on Central Nervous System Inflammation

描述(由申请人提供)：近年来，免疫和炎症机制对急性和慢性中枢神经系统(CNS)疾病的影响显著增加。炎症介质和细胞过程曾被认为仅限于外周免疫反应，现在已知在许多重要的中枢神经系统疾病的发病机制中起核心作用，如多发性硬化症、阿尔茨海默病、中风、艾滋病毒痴呆等。免疫细胞在大脑中的招募和调节是由中枢神经系统环境塑造的，在中枢神经系统环境中，小胶质细胞和星形胶质细胞等细胞阐述了各种强大的调节介质。这些介体包括一系列不断扩大的细胞因子、趋化因子、蛋白水解酶以及补体蛋白和活性氧物种。随着转基因和基因敲除动物模型的发展，确定这些介质在中枢神经系统疾病中的作用已经有了很大的进步。这些动物模型在许多情况下提供了意想不到的结果，从而拓宽了我们对中枢神经系统炎症机制的理解。这次多学科会议将通过四个具体目标讨论中枢神经系统免疫和炎症性疾病的基本机制、模型方法和新疗法的最新进展：1)检查分子和细胞效应物如何共同促进中枢神经系统的渗透和炎症；2)探索炎症和神经变性的复杂关系-炎症在中枢神经系统中总是有害的吗？3)比较和对比病原体和宿主诱导的炎症的机制，以及4)检查慢性炎症性疾病中免疫调节的争议和风险。会议项目由不同的调查人员组成(超过45%是女性、少数民族或年轻调查人员)，只有不到40%的项目演讲者接受了NIH的资助。

DESCRIPTION (provided by applicant): Knowledge of the immunologic and inflammatory mechanisms contributing to acute and chronic central nervous system (CNS) diseases has increased dramatically in recent years. Inflammatory mediators and cellular processes once thought to be restricted to peripheral immune responses are now known to be central to the pathogenesis of many important CNS diseases, such as multiple sclerosis, Alzheimer's disease, stroke, HIV-dementia and others. Immune cell recruitment and regulation in the brain is molded by the CNS environment, in which cells such as microglia and astrocytes, elaborate a variety of potent regulatory mediators. The mediators include an expanding array of cytokines, chemokines, proteases, as well as, complement proteins and reactive oxygen species. Determining the role of these mediators in CNS disease has been advanced considerably by the development of transgenic and knock-out animal models. These animal models have, in many cases, provided unexpected results, thus broadening our understanding of inflammatory mechanisms in the CNS. This multi-disciplinary meeting will address recent advances in basic mechanisms, model approaches and novel therapies in immunologic and inflammatory diseases of the CNS through four specific aims: 1) Examination of how molecular and cellular effectors jointly contribute to CNS infiltration and inflammation, 2) Exploration of the complex relationship of inflammation and neurodegeneration - is inflammation always detrimental in the CNS?, 3) Comparing and contrasting the mechanisms of pathogen- versus host-induced inflammation and, 4) Examination of the controversy and risk of immunomodulation in chronic inflammatory diseases. The meeting program is composed of a diverse group of investigators (over 45% are women, ethnic minorities or young investigators) and less than 40% of the program speakers receive NIH funding.