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.
