title: The good and the bad of neuroinflammation in multiple sclerosis.
abstract: Multiple sclerosis (MS) is the most common inflammatory, demyelinating, neurodegenerative disorder of the central nervous system (CNS). It is widely considered a T-cell mediated autoimmune disease that develops in genetically susceptible individuals, possibly under the influence of certain environmental trigger factors. The invasion of autoreactive CD4+ T-cells into the CNS is thought to be a central step that initiates the disease. Several other cell types, including CD8+ T-cells, B-cells and phagocytes appear to be involved in causing inflammation and eventually neurodegeneration. But inflammation is not entirely deleterious in MS. Evidence has accumulated in the recent years that show the importance of regulatory immune mechanisms which restrain tissue damage and initiate regeneration. More insight into the beneficial aspects of neuroinflammation might allow us to develop new treatment strategies for this enigmatic disease.
authors: Institute for Neuroimmunology and Clinical Multiple Sclerosis Research, Center for Molecular Neurobiology Hamburg, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
authors: Matthias
authors: M
authors: Naegele
authors: Neuroimmunology and MS Research, Neurology Clinic, University Hospital, Zurich, Switzerland. Electronic address: roland.martin@usz.ch.
authors: Roland
authors: R
authors: Martin
mesh_terms: D000818:Animals; D002490:Central Nervous System / Q000276:immunology; D004195:Disease Models, Animal; D006801:Humans; D007249:Inflammation / Q000276:immunology / Q000378:metabolism; D009103:Multiple Sclerosis / Q000209:etiology / Q000276:immunology* / Q000628:therapy; D019636:Neurodegenerative Diseases / Q000276:immunology / Q000378:metabolism*; D015398:Signal Transduction
keywords: axons; blood-brain barrier; demyelination; inflammation; inflammatory cascade; injury; myelin; remyelination; repair; tissue injury