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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
8
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pubmed:dateCreated |
2002-10-22
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pubmed:abstractText |
We previously described a mechanism for the maintenance of peripheral self-tolerance. This involves the cross-presentation of tissue-associated antigens by a bone marrow-derived cell type that stimulates the proliferation and ultimate deletion of self-reactive CD8 T cells. This process has been referred to as cross-tolerance. Here, we characterize the elusive cell type responsible for inducing cross-tolerance as a CD8alpha(+) dendritic cell (DC). To achieve this aim, transgenic mice were generated expressing yellow fluorescent protein (YFP) linked to CTL epitopes for ovalbumin and glycoprotein B (gB) of herpes simplex virus under the rat insulin promoter (RIP). Although tracking of YFP was inconclusive, the use of a highly sensitive gB-specific hybridoma that produced beta-galactosidase on encounter with antigen, enabled detection of antigen presentation by cells isolated from the pancreatic lymph node. This showed that a CD11c(+)CD8alpha(+) cell was responsible for cross-tolerance, the same DC subset as previously implicated in cross-priming. These data indicate that CD8alpha(+) DCs play a critical role in both tolerance and immunity to cell-associated antigens, providing a potential mechanism by which cytotoxic T lymphocyte can be immunized to viral antigens while maintaining tolerance to self.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-10535986,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-10580495,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-1083422,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-11120766,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-11160180,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-11244030,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-11342628,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-11441078,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-11560993,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-11773639,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-11869679,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-11877488,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-11905820,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-11940116,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-12021304,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-12021309,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-12391012,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-1378619,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-1613465,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-1739426,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-3029267,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-8011301,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-8287475,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-9064352,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-9206998,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-9221753,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-9624004,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-9624005,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-9670054,
http://linkedlifedata.com/resource/pubmed/commentcorrection/12391021-9850866
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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 |
Oct
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pubmed:issn |
0022-1007
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pubmed:author |
pubmed-author:BehrensGeorg M NGM,
pubmed-author:BelzGabrielle TGT,
pubmed-author:CarboneFrancis RFR,
pubmed-author:FathmanC GarrisonCG,
pubmed-author:HeathWilliam RWR,
pubmed-author:JonesClaerwenC,
pubmed-author:LejonKristinaK,
pubmed-author:MillerJacques F A PJF,
pubmed-author:MuellerScott NSN,
pubmed-author:ShortmanKenK,
pubmed-author:SmithChris MCM
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pubmed:issnType |
Print
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pubmed:day |
21
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pubmed:volume |
196
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1099-104
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:12391021-Animals,
pubmed-meshheading:12391021-Antigens, CD,
pubmed-meshheading:12391021-Bacterial Proteins,
pubmed-meshheading:12391021-Base Sequence,
pubmed-meshheading:12391021-CD8-Positive T-Lymphocytes,
pubmed-meshheading:12391021-DNA Primers,
pubmed-meshheading:12391021-Immune Tolerance,
pubmed-meshheading:12391021-Immunophenotyping,
pubmed-meshheading:12391021-Insulin,
pubmed-meshheading:12391021-Luminescent Proteins,
pubmed-meshheading:12391021-Mice,
pubmed-meshheading:12391021-Mice, Transgenic,
pubmed-meshheading:12391021-Promoter Regions, Genetic,
pubmed-meshheading:12391021-Rats
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pubmed:year |
2002
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pubmed:articleTitle |
The CD8alpha(+) dendritic cell is responsible for inducing peripheral self-tolerance to tissue-associated antigens.
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pubmed:affiliation |
Immunology Division, The Walter and Eliza Hall Institute of Medical Research, Victoria 3050, Australia. belz@wehi.edu.au
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pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
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