Increased reactivity to myelin oligodendrocyte glycoprotein peptides and epitope mapping in HLA DR2(15)+ multiple sclerosis
Multiple sclerosis (MS) is a central nervous system‐specific inflammatory and demyelinating disease where a myelin‐directed autoimmune response is thought to be pathogenetically relevant. Myelin oligodendrocyte glycoprotein (MOG) is a surface‐exposed minor myelin component that is a prime candidate...
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Published in | European journal of immunology Vol. 28; no. 10; pp. 3329 - 3335 |
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Main Authors | , , , , , |
Format | Journal Article |
Language | English |
Published |
Weinheim
WILEY‐VCH Verlag GmbH
01.10.1998
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Subjects | |
Online Access | Get full text |
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Summary: | Multiple sclerosis (MS) is a central nervous system‐specific inflammatory and demyelinating disease where a myelin‐directed autoimmune response is thought to be pathogenetically relevant. Myelin oligodendrocyte glycoprotein (MOG) is a surface‐exposed minor myelin component that is a prime candidate autoantigen. We have investigated peripheral blood lymphocyte responses to synthetic 15 – 26 amino acids long overlapping MOG peptides in 20 MS patients and 14 healthy controls with the MS‐associated HLA haplotype DR2(15). There were significantly increased responses, in terms of numbers of cells secreting IFN‐γ detected by Elispot in response to several MOG‐derived peptides in the MS patients, but not the healthy controls. MOG peptide 63 – 87 evoked the strongest response, and the stimulatory property of this peptide was confirmed in additional DR2(15)+ MS patients where a peptide concentration‐dependent proliferative response, which was inhibited by the addition of anti‐HLA class II antibodies, was observed. This is the first work detailing putative immunodominant T cell epitopes of MOG in DR2(15)+ MS patients. |
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Bibliography: | ObjectType-Article-2 SourceType-Scholarly Journals-1 ObjectType-Feature-1 content type line 23 ObjectType-Article-1 ObjectType-Feature-2 |
ISSN: | 0014-2980 1521-4141 |
DOI: | 10.1002/(SICI)1521-4141(199810)28:10<3329::AID-IMMU3329>3.0.CO;2-B |