Source:http://linkedlifedata.com/resource/pubmed/id/11500819
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions | |
| pubmed:issue |
8
|
| pubmed:dateCreated |
2001-8-13
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| pubmed:abstractText |
Antigen-driven development of persistent self-reactive Th cells underlies the chronic, progressive nature of many autoimmune diseases. It is crucial to understand the behavior of these self-reactive Th cells; however, they have been notoriously difficult to isolate directly ex vivo. Collagen-induced arthritis (CIA) can be initiated in I-A(q)-expressing mice (DBA/1) using heterologous type II collagen (cII) immunization and is dependent on Th cells that are specific for a single immunodominant epitope. Here, we identify one compartment of cII-specific Th cell using TCR beta expression, cell surface phenotype, and direct single-cell repertoire analysis. A subpopulation of CD4(+)V beta 10(+) T cells up-regulates both CD44 and GL7 and expands significantly in response to initial priming in the majority of animals (D9: 70%). The cII-specific V beta 10(+) primary responders are further resolved through expression of a highly restricted junctional region, previously associated with autoimmune disease. This cII-specific clonotype rapidly re-expands upon antigen recall and can be isolated from the lymph nodes of arthritic animals. These single-cell analyses quantify the emergence, decline and rapid re-emergence of a self-reactive Th cell population in vivo and outline one strategy for isolating these cells directly ex vivo.
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| pubmed:grant | |
| pubmed:language |
eng
|
| pubmed:journal | |
| pubmed:citationSubset |
IM
|
| pubmed:chemical | |
| pubmed:status |
MEDLINE
|
| pubmed:month |
Aug
|
| pubmed:issn |
0014-2980
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| pubmed:author | |
| pubmed:issnType |
Print
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| pubmed:volume |
31
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| pubmed:owner |
NLM
|
| pubmed:authorsComplete |
Y
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| pubmed:pagination |
2362-72
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| pubmed:dateRevised |
2007-11-14
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| pubmed:meshHeading |
pubmed-meshheading:11500819-Amino Acid Sequence,
pubmed-meshheading:11500819-Animals,
pubmed-meshheading:11500819-Arthritis,
pubmed-meshheading:11500819-Autoimmune Diseases,
pubmed-meshheading:11500819-Autoimmunity,
pubmed-meshheading:11500819-Base Sequence,
pubmed-meshheading:11500819-Clone Cells,
pubmed-meshheading:11500819-Collagen,
pubmed-meshheading:11500819-Complementarity Determining Regions,
pubmed-meshheading:11500819-Flow Cytometry,
pubmed-meshheading:11500819-Immunization,
pubmed-meshheading:11500819-Immunologic Memory,
pubmed-meshheading:11500819-Lymphocyte Activation,
pubmed-meshheading:11500819-Male,
pubmed-meshheading:11500819-Mice,
pubmed-meshheading:11500819-Mice, Inbred DBA,
pubmed-meshheading:11500819-Molecular Sequence Data,
pubmed-meshheading:11500819-RNA, Messenger,
pubmed-meshheading:11500819-Receptors, Antigen, T-Cell,
pubmed-meshheading:11500819-Substrate Specificity,
pubmed-meshheading:11500819-T-Lymphocytes, Helper-Inducer
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| pubmed:year |
2001
|
| pubmed:articleTitle |
Emergence of a type II collagen-specific helper T cell response.
|
| pubmed:affiliation |
Department of Immunology, Duke University Medical Center, Durham, NC 27704, USA.
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| pubmed:publicationType |
Journal Article,
Research Support, U.S. Gov't, P.H.S.,
Research Support, Non-U.S. Gov't
|