Source:http://linkedlifedata.com/resource/pubmed/id/11544345
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
6
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pubmed:dateCreated |
2001-9-6
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pubmed:abstractText |
Numerous clinical and epidemiological studies link enteroviruses such as the Coxsackie virus group with the autoimmune disease type 1 diabetes mellitus (DM). In addition, there are reports that patients with type 1 DM are characterized by skewing of TCR Vbeta chain selection among peripheral blood and intraislet T lymphocytes. To examine these issues, we analyzed TCR Vbeta chain-specific up-regulation of the early T cell activation marker, CD69, on CD4 T cells after incubation with Coxsackievirus B4 (CVB4) Ags. CD4 T cells bearing the Vbeta chains 2, 7, and 8 were the most frequently activated by CVB4. Up-regulation of CD69 by different TCR families was significantly more frequent in new onset type 1 DM patients (p = 0.04), 100% of whom (n = 8) showed activation of CD4 T cells bearing Vbeta8, compared with 50% of control subjects (n = 8; p = 0.04). T cell proliferation after incubation with CVB4 Ags required live, nonfixed APCs, suggesting that the selective expansion of CD4 T cells with particular Vbeta chains resulted from conventional antigen processing and presentation rather than superantigen activity. Heteroduplex analysis of TCR Vbeta chain usage after CVB4 stimulation indicated a relatively polyclonal, rather than oligo- or monoclonal response to viral Ags. These results provide evidence that new-onset patients with type 1 DM and healthy controls are primed against CVB4, and that CD4 T cell responses to the virus have a selective TCR Vbeta chain usage which is driven by viral Ags rather than a superantigen.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
AIM
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pubmed:chemical |
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Differentiation...,
http://linkedlifedata.com/resource/pubmed/chemical/Antigens, Viral,
http://linkedlifedata.com/resource/pubmed/chemical/CD69 antigen,
http://linkedlifedata.com/resource/pubmed/chemical/Lectins, C-Type,
http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Antigen, T-Cell...,
http://linkedlifedata.com/resource/pubmed/chemical/Superantigens
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pubmed:status |
MEDLINE
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pubmed:month |
Sep
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pubmed:issn |
0022-1767
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
167
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3513-20
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pubmed:dateRevised |
2010-11-18
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pubmed:meshHeading |
pubmed-meshheading:11544345-Adult,
pubmed-meshheading:11544345-Antigen Presentation,
pubmed-meshheading:11544345-Antigen-Presenting Cells,
pubmed-meshheading:11544345-Antigens, CD,
pubmed-meshheading:11544345-Antigens, Differentiation, T-Lymphocyte,
pubmed-meshheading:11544345-Antigens, Viral,
pubmed-meshheading:11544345-Autoimmune Diseases,
pubmed-meshheading:11544345-CD4-Positive T-Lymphocytes,
pubmed-meshheading:11544345-Cell Division,
pubmed-meshheading:11544345-Coculture Techniques,
pubmed-meshheading:11544345-Diabetes Mellitus, Type 1,
pubmed-meshheading:11544345-Enterovirus B, Human,
pubmed-meshheading:11544345-Enterovirus Infections,
pubmed-meshheading:11544345-Female,
pubmed-meshheading:11544345-Gene Rearrangement, beta-Chain T-Cell Antigen Receptor,
pubmed-meshheading:11544345-Heteroduplex Analysis,
pubmed-meshheading:11544345-Humans,
pubmed-meshheading:11544345-Lectins, C-Type,
pubmed-meshheading:11544345-Lymphocyte Activation,
pubmed-meshheading:11544345-Male,
pubmed-meshheading:11544345-Receptors, Antigen, T-Cell, alpha-beta,
pubmed-meshheading:11544345-Superantigens,
pubmed-meshheading:11544345-T-Lymphocyte Subsets,
pubmed-meshheading:11544345-Up-Regulation
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pubmed:year |
2001
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pubmed:articleTitle |
T cell activation by coxsackievirus B4 antigens in type 1 diabetes mellitus: evidence for selective TCR Vbeta usage without superantigenic activity.
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pubmed:affiliation |
Department of Immunology, Guy's, King's and St. Thomas' School of Medicine, London, United Kingdom.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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