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Multiple sclerosis: MHC associations and therapeutic implications

Published online by Cambridge University Press:  14 February 2005

Samantha Holmes
Affiliation:
Division of Structural Biology, The Henry Wellcome Building for Genomic Medicine, The University of Oxford, Roosevelt Drive, Oxford, OX3 7BN, UK.
Manuel A. Friese
Affiliation:
MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, The University of Oxford, Oxford, OX3 9DS, UK.
Christian Siebold
Affiliation:
Division of Structural Biology, The Henry Wellcome Building for Genomic Medicine, The University of Oxford, Roosevelt Drive, Oxford, OX3 7BN, UK.
E. Yvonne Jones
Affiliation:
Division of Structural Biology, The Henry Wellcome Building for Genomic Medicine, The University of Oxford, Roosevelt Drive, Oxford, OX3 7BN, UK.
John Bell
Affiliation:
Nuffield Dept of Clinical Medicine, John Radcliffe Hospital, The University of Oxford, Oxford, OX3 9DU, UK.
Lars Fugger
Affiliation:
MRC Human Immunology Unit, Weatherall Institute of Molecular Medicine, John Radcliffe Hospital, The University of Oxford, Oxford, OX3 9DS, UK.
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Abstract

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Multiple sclerosis (MS) is an autoimmune disease with an important genetic component. The strongest genetic association is with the major histocompatibility complex (MHC) region. Several MHC alleles predispose to the disease, the most prominent of which are certain alleles in the HLA-DR2 haplotype. Functional and structural studies have helped to explain the molecular basis of these associations. Although there is currently no curative treatment for MS, an increased understanding of the disease has aided the design of immunotherapies that act on the immune system more specifically than the longstanding drugs. Many of these therapies work at the antigen-specific level, disrupting the interaction between T-cell receptors and MHC molecules that leads to disease.

Type
Review Article
Copyright
© Cambridge University Press 2005