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Inflamed Brains: Neuroimmune Interactions in Diseases of the Nervous System Fondation IPSEN, Paris, France October 5, 1998

In the past ten years, the brain’s status as “immune privileged,” that is, beyond the surveillance and influence of the immune system, has been reconsidered as important interactions between the nervous and immune systems have been recognized. Increasing attention is being paid to the role of inflammatory responses in degenerative diseases of the brain, particularly in Aizheimer’s disease, as well as in trauma and even in mental illness. The Autumn Colloque of the Fondation IPSEN (Neuroimmune Interactions in Diseases of the Nervous System) held on October 6, 1998 in Paris, was organized by P. Patterson (Pasadena, USA), C. Kordon (Paris, France), and Y. Christen (Paris, France). This meeting brought together researchers in immunology and neuroscience to discuss progress and to identify areas for future collaboration. The healthy central nervous system does indeed lack the classic immunological antibody response for neutralizing foreign proteins found in the rest of the body. But it has long been known that, when faced with certain insults, the nervous system can produce a modified inflammatory response, as in multiple sclerosis (H. Wekerle, Max-Planck-Institut für Neurobiologie, Planegg-Martinsried, Germany). More recently, the macrophages and lymphocytes of the immune system have been shown to patrol the healthy brain and to invade it in large numbers when disease threatens. Outside the brain, injury or infection triggers macrophages and lymphocytes to produce a complex cascade of chemical and cellular reactions that results in inflammation, which both protects against the insult and then promotes repair. In a bad infection, there may be fever and the behavior pattern associated with sickness. The acute response is usually short lasting as it is balanced by mechanisms restoring the body to health. Occasionally, for reasons that are not well understood, the restorative process fails and a chronic, pathological inflammation persists — typified by arthritis. Attention to neuroimmune interactions leading to inflammation in the brain increased when many classes of molecule associated with the peripheral inflammatory response were discovered in association with amyloid plaques in the brains of patients with Alzheimer’s disease (AD). This may be a sign of a chronic inflammatory condition, according to P. McGeer (Univ. British Columbia, Vancouver, Canada), one pioneer of this concept. Now it seems likely that even psychiatric conditions such as major depression may have an inflammatory component.