rdf:type |
|
lifeskim:mentions |
|
pubmed:issue |
7
|
pubmed:dateCreated |
2001-3-29
|
pubmed:abstractText |
Antigens of pathogenic microbes that mimic autoantigens are thought to be responsible for the activation of autoreactive T cells. Viral infections have been associated with the development of the neuroendocrine autoimmune diseases type 1 diabetes and stiff-man syndrome, but the mechanism is unknown. These diseases share glutamic acid decarboxylase (GAD65) as a major autoantigen. We screened synthetic peptide libraries dedicated to bind to HLA-DR3, which predisposes to both diseases, using clonal CD4(+) T cells reactive to GAD65 isolated from a prediabetic stiff-man syndrome patient. Here we show that these GAD65-specific T cells crossreact with a peptide of the human cytomegalovirus (hCMV) major DNA-binding protein. This peptide was identified after database searching with a recognition pattern that had been deduced from the library studies. Furthermore, we showed that hCMV-derived epitope can be naturally processed by dendritic cells and recognized by GAD65 reactive T cells. Thus, hCMV may be involved in the loss of T cell tolerance to autoantigen GAD65 by a mechanism of molecular mimicry leading to autoimmunity.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/11274421-10330300,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11274421-10679401,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11274421-1309355,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11274421-1697648,
http://linkedlifedata.com/resource/pubmed/commentcorrection/11274421-1901764,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/11274421-9802984
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pubmed:language |
eng
|
pubmed:journal |
|
pubmed:citationSubset |
IM
|
pubmed:chemical |
|
pubmed:status |
MEDLINE
|
pubmed:month |
Mar
|
pubmed:issn |
0027-8424
|
pubmed:author |
pubmed-author:BehanP OPO,
pubmed-author:ChaudhuriAA,
pubmed-author:DrijfhoutJ WJW,
pubmed-author:FrankenK LKL,
pubmed-author:HiemstraH SHS,
pubmed-author:RoepB OBO,
pubmed-author:SchlootN CNC,
pubmed-author:WillemenS JSJ,
pubmed-author:de VriesR RRR,
pubmed-author:van RoodJ JJJ,
pubmed-author:van VeelenP APA
|
pubmed:issnType |
Print
|
pubmed:day |
27
|
pubmed:volume |
98
|
pubmed:owner |
NLM
|
pubmed:authorsComplete |
Y
|
pubmed:pagination |
3988-91
|
pubmed:dateRevised |
2009-11-18
|
pubmed:meshHeading |
pubmed-meshheading:11274421-Antigens, Viral,
pubmed-meshheading:11274421-Autoantibodies,
pubmed-meshheading:11274421-Autoantigens,
pubmed-meshheading:11274421-Autoimmunity,
pubmed-meshheading:11274421-Cross Reactions,
pubmed-meshheading:11274421-Cytomegalovirus,
pubmed-meshheading:11274421-Epitopes,
pubmed-meshheading:11274421-Glutamate Decarboxylase,
pubmed-meshheading:11274421-Humans,
pubmed-meshheading:11274421-T-Lymphocytes
|
pubmed:year |
2001
|
pubmed:articleTitle |
Cytomegalovirus in autoimmunity: T cell crossreactivity to viral antigen and autoantigen glutamic acid decarboxylase.
|
pubmed:affiliation |
Department of Immunohematology and Blood Transfusion, Leiden University Medical Center, P. O. Box 9600, NL-2300 RC Leiden, The Netherlands.
|
pubmed:publicationType |
Journal Article,
In Vitro,
Research Support, Non-U.S. Gov't
|