Multiple Sclerosis: Are Protective Immune Mechanisms Compromised by a Complex Infectious Background?

The immunological background of multiple sclerosis (MS) manifests as an altered reactivity against a diverse range of infections, particularly with the Epstein-Barr virus. Although this could be only an epiphenomenon of a more generalised dysfunction of the immune system in MS, it is also possible t...

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Main Authors: Bernd Krone, John M. Grange
Format: Article
Language:English
Published: Hindawi Limited 2011-01-01
Series:Autoimmune Diseases
Online Access:http://dx.doi.org/10.4061/2011/708750
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spelling doaj-b91804cbd9dc4f0092911dc27be000ae2020-11-25T01:41:19ZengHindawi LimitedAutoimmune Diseases2090-04302011-01-01201110.4061/2011/708750708750Multiple Sclerosis: Are Protective Immune Mechanisms Compromised by a Complex Infectious Background?Bernd Krone0John M. Grange1Institute of Virology, Centre for Hygiene and Human Genetics, University of Göttingen, Kreuzbergring 57, 37075 Göttingen, GermanyAdvanced Therapies Centre B2, London Clinic Cancer Centre, 22 Devonshire Place, London W1G 6JA, UKThe immunological background of multiple sclerosis (MS) manifests as an altered reactivity against a diverse range of infections, particularly with the Epstein-Barr virus. Although this could be only an epiphenomenon of a more generalised dysfunction of the immune system in MS, it is also possible that a complex infectious background forms the basis of a specific immune dysregulation finally causing the disease. It is thus suggested that the complex infectious background bears the key for an understanding of the immune pathogenesis of the disease. It appears probable that improved standards of hygiene cause regulatory defects in the immune system, allowing the abnormal expression of human endogenous retroviral (HERV) genes. On the basis of epidemiological observations we describe how a failure of expansion or an eclipse of a subfraction of self-antigen-specific CD8+ T cells mediating immune repair, and a deleterious mode of action of HERV gene products, could underlie the pathogenesis of MS.http://dx.doi.org/10.4061/2011/708750
collection DOAJ
language English
format Article
sources DOAJ
author Bernd Krone
John M. Grange
spellingShingle Bernd Krone
John M. Grange
Multiple Sclerosis: Are Protective Immune Mechanisms Compromised by a Complex Infectious Background?
Autoimmune Diseases
author_facet Bernd Krone
John M. Grange
author_sort Bernd Krone
title Multiple Sclerosis: Are Protective Immune Mechanisms Compromised by a Complex Infectious Background?
title_short Multiple Sclerosis: Are Protective Immune Mechanisms Compromised by a Complex Infectious Background?
title_full Multiple Sclerosis: Are Protective Immune Mechanisms Compromised by a Complex Infectious Background?
title_fullStr Multiple Sclerosis: Are Protective Immune Mechanisms Compromised by a Complex Infectious Background?
title_full_unstemmed Multiple Sclerosis: Are Protective Immune Mechanisms Compromised by a Complex Infectious Background?
title_sort multiple sclerosis: are protective immune mechanisms compromised by a complex infectious background?
publisher Hindawi Limited
series Autoimmune Diseases
issn 2090-0430
publishDate 2011-01-01
description The immunological background of multiple sclerosis (MS) manifests as an altered reactivity against a diverse range of infections, particularly with the Epstein-Barr virus. Although this could be only an epiphenomenon of a more generalised dysfunction of the immune system in MS, it is also possible that a complex infectious background forms the basis of a specific immune dysregulation finally causing the disease. It is thus suggested that the complex infectious background bears the key for an understanding of the immune pathogenesis of the disease. It appears probable that improved standards of hygiene cause regulatory defects in the immune system, allowing the abnormal expression of human endogenous retroviral (HERV) genes. On the basis of epidemiological observations we describe how a failure of expansion or an eclipse of a subfraction of self-antigen-specific CD8+ T cells mediating immune repair, and a deleterious mode of action of HERV gene products, could underlie the pathogenesis of MS.
url http://dx.doi.org/10.4061/2011/708750
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