pubmed-article:12391021 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:12391021 | lifeskim:mentions | umls-concept:C1273518 | lld:lifeskim |
pubmed-article:12391021 | lifeskim:mentions | umls-concept:C0011306 | lld:lifeskim |
pubmed-article:12391021 | lifeskim:mentions | umls-concept:C0003320 | lld:lifeskim |
pubmed-article:12391021 | lifeskim:mentions | umls-concept:C0205100 | lld:lifeskim |
pubmed-article:12391021 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:12391021 | pubmed:issue | 8 | lld:pubmed |
pubmed-article:12391021 | pubmed:dateCreated | 2002-10-22 | lld:pubmed |
pubmed-article:12391021 | 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. | lld:pubmed |
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pubmed-article:12391021 | pubmed:language | eng | lld:pubmed |
pubmed-article:12391021 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:12391021 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:12391021 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:12391021 | pubmed:month | Oct | lld:pubmed |
pubmed-article:12391021 | pubmed:issn | 0022-1007 | lld:pubmed |
pubmed-article:12391021 | pubmed:author | pubmed-author:ShortmanKenK | lld:pubmed |
pubmed-article:12391021 | pubmed:author | pubmed-author:MuellerScott... | lld:pubmed |
pubmed-article:12391021 | pubmed:author | pubmed-author:HeathWilliam... | lld:pubmed |
pubmed-article:12391021 | pubmed:author | pubmed-author:CarboneFranci... | lld:pubmed |
pubmed-article:12391021 | pubmed:author | pubmed-author:BelzGabrielle... | lld:pubmed |
pubmed-article:12391021 | pubmed:author | pubmed-author:SmithChris... | lld:pubmed |
pubmed-article:12391021 | pubmed:author | pubmed-author:FathmanC... | lld:pubmed |
pubmed-article:12391021 | pubmed:author | pubmed-author:MillerJacques... | lld:pubmed |
pubmed-article:12391021 | pubmed:author | pubmed-author:BehrensGeorg... | lld:pubmed |
pubmed-article:12391021 | pubmed:author | pubmed-author:JonesClaerwen... | lld:pubmed |
pubmed-article:12391021 | pubmed:author | pubmed-author:LejonKristina... | lld:pubmed |
pubmed-article:12391021 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:12391021 | pubmed:day | 21 | lld:pubmed |
pubmed-article:12391021 | pubmed:volume | 196 | lld:pubmed |
pubmed-article:12391021 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:12391021 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:12391021 | pubmed:pagination | 1099-104 | lld:pubmed |
pubmed-article:12391021 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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pubmed-article:12391021 | pubmed:year | 2002 | lld:pubmed |
pubmed-article:12391021 | pubmed:articleTitle | The CD8alpha(+) dendritic cell is responsible for inducing peripheral self-tolerance to tissue-associated antigens. | lld:pubmed |
pubmed-article:12391021 | pubmed:affiliation | Immunology Division, The Walter and Eliza Hall Institute of Medical Research, Victoria 3050, Australia. belz@wehi.edu.au | lld:pubmed |
pubmed-article:12391021 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:12391021 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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