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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
4
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pubmed:dateCreated |
1999-7-30
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pubmed:abstractText |
Monoclonal antibodies (mAb) specific for the clonotype of an autoreactive T cell may be useful reagents in the modulation of autoimmune disease. We have previously reported the generation of a set of mAb specific for the clonotypic structure of a human T-cell clone recognizing an epitope of human cartilage gp-39. This glycoprotein was recently identified as a candidate autoantigen in rheumatoid arthritis. Here, we demonstrate for the first time that small amounts of immobilized anticlonotype mAb can induce anergy in the autoreactive clone. Following the anergic stimulus, T cells failed to proliferate upon restimulation as a result of a lack of interleukin-2 (IL-2) gene transcription. In addition, a diminished interferon-gamma (IFN-gamma) production was found. Our data indicate that anergy was not a result of T-cell receptor (TCR) downmodulation or the absence of free TCR. The anergic state was induced independent of costimulation or the presence of IL-2 and no protein synthesis was required for the induction of anergy. Anticlonotype mAb-induced anergy was prevented by cyclosporin A, suggesting that active signalling via the calcium/calcineurin pathway was required for the induction of anergy. In coculture experiments, anergic T cells were found to suppress the response of reactive cells from the same clone. This bystander suppression led to 90% inhibition of peptide-induced proliferation. Together, these findings suggest that mAb to the clonotypic structure of autoreactive T cells may be suitable reagents for the functional inactivation of these T cells in autoimmune diseases.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-1387666,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-1432162,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-1512550,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-1893964,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-2153162,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-2457547,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-3035012,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-7500045,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-7507511,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-7680433,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-7858528,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-7878934,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-7968257,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-7973657,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-8003614,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-8011155,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-8040252,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-8088317,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-8202711,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-8254420,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-8360588,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-8483498,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-8485907,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-8606766,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-8608651,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-8609395,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-8610163,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-8647186,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-8658175,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-8691122,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-8757610,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-8790400,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-8892873,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-8921948,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-9243292,
http://linkedlifedata.com/resource/pubmed/commentcorrection/10233745-9502584
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Apr
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pubmed:issn |
0019-2805
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:volume |
96
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
586-94
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pubmed:dateRevised |
2009-11-18
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pubmed:meshHeading |
pubmed-meshheading:10233745-Antibodies, Monoclonal,
pubmed-meshheading:10233745-Antigen-Presenting Cells,
pubmed-meshheading:10233745-Cell Culture Techniques,
pubmed-meshheading:10233745-Cell Survival,
pubmed-meshheading:10233745-Clonal Anergy,
pubmed-meshheading:10233745-Cycloheximide,
pubmed-meshheading:10233745-Cyclosporine,
pubmed-meshheading:10233745-Humans,
pubmed-meshheading:10233745-Immunosuppressive Agents,
pubmed-meshheading:10233745-Interferon-gamma,
pubmed-meshheading:10233745-Interleukin-2,
pubmed-meshheading:10233745-Receptors, Antigen, T-Cell,
pubmed-meshheading:10233745-T-Lymphocytes,
pubmed-meshheading:10233745-Time Factors,
pubmed-meshheading:10233745-Transcription, Genetic
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pubmed:year |
1999
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pubmed:articleTitle |
T-cell anergy induced by clonotype-specific antibodies: modulation of an autoreactive human T-cell clone in vitro.
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pubmed:affiliation |
Department of Immunology, N. V. Organon, Oss, The Netherlands.
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pubmed:publicationType |
Journal Article
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