Virus-mediated autoimmunity in Multiple Sclerosis
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BioMed Central
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Virus-mediated autoimmunity in Multiple Sclerosis Nikolaos Grigoriadis1 and Georgios M Hadjigeorgiou*2 Address: 1B' Department of Neurology, Laboratory of Experimental Neurology and Neuroimmunology, AHEPA University Hospital, 1 Stilp Kyriakidi Street, Aristotle University of Thessaloniki, Thessaloniki, 54636 Thessaloniki, Greece and 2Department of Neurology, Neurogenetics Unit, Medical School, University of Thessaly, 22 Papakyriazi Street, 41222 Larissa, Greece Email: Nikolaos Grigoriadis - [email protected]; Georgios M Hadjigeorgiou* - [email protected] * Corresponding author
Published: 19 February 2006 Journal of Autoimmune Diseases 2006, 3:1
doi:10.1186/1740-2557-3-1
Received: 31 October 2005 Accepted: 19 February 2006
This article is available from: http://www.jautoimdis.com/content/3/1/1 © 2006 Grigoriadis and Hadjgeorgiou; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.
Abstract Epidemiological data suggest the notion that in Multiple Sclerosis (MS) is an acquired autoimmune disease and the cause may be an environmental factor(s), probably infectious, in genetically susceptible individuals. Several cases of viral induced demyelinatimg encephalomyelitis in human beings and in experimental models as well as the presence of IgG oligoclonal bands in the cerebrospinal fluid indicate that the infectious factor may be viral. However, the absence of a specific virus identification in MS central nervous system may hardly support this notion. On the other hand, the partial response of patients with MS to immunosuppressive and immunomodulatory therapy support the evidence of an autoimmune etiology for MS. However, the autoimmune hypothesis shares the same criticism with the infectious one in that no autoantigen(s) specific to and causative for MS has ever been identified. Nevertheless, the absence of identifiable infectious agent, especially viral does not rule out its presence at a certain time – point and the concomitant long term triggering of an autoimmune cascade of events thereafter. Several concepts have emerged in an attempt to explain the autoimmune mechanisms and ongoing neurodegeneration in MS on the basis of the infectious – viral hypothesis.
Background Multiple sclerosis (MS) is widely believed to be an autoimmune disorder characterized by multifocal lesions of the CNS myelin and accumulating clinical signs due to axonal damage [1]. The aetiology of MS has been debated several times since the disease was first described. Myelin is damaged due to an immune attack consisted of several pathways and molecules, leading to impaired nerve function. Autoantibodies and autoreactive T cells activated against myelin antigens such as myelin basic protein (MBP), proteolipid protein (PLP), and myelin oligodendrocyte glycoprot
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