| pubmed-article:15368281 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:15368281 | lifeskim:mentions | umls-concept:C0085243 | lld:lifeskim |
| pubmed-article:15368281 | lifeskim:mentions | umls-concept:C0567416 | lld:lifeskim |
| pubmed-article:15368281 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
| pubmed-article:15368281 | lifeskim:mentions | umls-concept:C1704410 | lld:lifeskim |
| pubmed-article:15368281 | lifeskim:mentions | umls-concept:C1145667 | lld:lifeskim |
| pubmed-article:15368281 | lifeskim:mentions | umls-concept:C1510827 | lld:lifeskim |
| pubmed-article:15368281 | lifeskim:mentions | umls-concept:C0205251 | lld:lifeskim |
| pubmed-article:15368281 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
| pubmed-article:15368281 | pubmed:issue | 10 | lld:pubmed |
| pubmed-article:15368281 | pubmed:dateCreated | 2004-9-15 | lld:pubmed |
| pubmed-article:15368281 | pubmed:databankReference | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15368281 | pubmed:abstractText | Although non-obese diabetic (NOD) mice spontaneously develop T cell autoimmunity, it is not clear whether this phenomenon results from a defect in tolerance to self-Ag. Furthermore, as autoimmunity has been postulated to result from T cell responses directed toward self-peptides that bind with low affinity to NOD I-A(g7) MHC class II molecules, it is important to determine whether the expression of such peptides induces tolerance. We have constructed NOD transgenic (Tg) mice expressing the Leishmania antigen receptor for C kinase (LACK) Ag in either the thymus or pancreatic beta cells. We identified LACK peptides that were the targets of T cells in LACK-immunized NOD mice while binding to I-A(g7) with low affinity. While CD4(+) T cells from NOD mice secreted IFN-gamma, IL-4, IL-5 and IL-10 in response to LACK, those from LACK-expressing Tg mice secreted reduced levels of cytokines. Experiments using peptide/MHC multimers showed that LACK-expressing Tg mice exhibited self-reactive CD4(+) T cells with impaired proliferation capabilities. Hence, even self-peptides that bind to I-A(g7) with low affinity can induce tolerance in NOD mice. This result is important in light of the commonly held hypothesis that T cells reacting to peptides that bind to MHC with low affinity escape tolerance induction and cause autoimmunity. | lld:pubmed |
| pubmed-article:15368281 | pubmed:language | eng | lld:pubmed |
| pubmed-article:15368281 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15368281 | pubmed:citationSubset | IM | lld:pubmed |
| pubmed-article:15368281 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15368281 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15368281 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15368281 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15368281 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15368281 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15368281 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15368281 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:15368281 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:15368281 | pubmed:month | Oct | lld:pubmed |
| pubmed-article:15368281 | pubmed:issn | 0014-2980 | lld:pubmed |
| pubmed-article:15368281 | pubmed:author | pubmed-author:LehuenAgnèsA | lld:pubmed |
| pubmed-article:15368281 | pubmed:author | pubmed-author:HuguesStéphan... | lld:pubmed |
| pubmed-article:15368281 | pubmed:author | pubmed-author:MougneauEvely... | lld:pubmed |
| pubmed-article:15368281 | pubmed:author | pubmed-author:BeaudoinLucie... | lld:pubmed |
| pubmed-article:15368281 | pubmed:author | pubmed-author:GlaichenhausN... | lld:pubmed |
| pubmed-article:15368281 | pubmed:author | pubmed-author:Wucherpfennig... | lld:pubmed |
| pubmed-article:15368281 | pubmed:author | pubmed-author:AppelHeinerH | lld:pubmed |
| pubmed-article:15368281 | pubmed:author | pubmed-author:JangMei-HueiM... | lld:pubmed |
| pubmed-article:15368281 | pubmed:author | pubmed-author:FerlinWalter... | lld:pubmed |
| pubmed-article:15368281 | pubmed:author | pubmed-author:CazarethJulie... | lld:pubmed |
| pubmed-article:15368281 | pubmed:author | pubmed-author:SchrickeCorin... | lld:pubmed |
| pubmed-article:15368281 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:15368281 | pubmed:volume | 34 | lld:pubmed |
| pubmed-article:15368281 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:15368281 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:15368281 | pubmed:pagination | 2656-63 | lld:pubmed |
| pubmed-article:15368281 | pubmed:dateRevised | 2006-11-15 | lld:pubmed |
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| pubmed-article:15368281 | pubmed:meshHeading | pubmed-meshheading:15368281... | lld:pubmed |
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| pubmed-article:15368281 | pubmed:meshHeading | pubmed-meshheading:15368281... | lld:pubmed |
| pubmed-article:15368281 | pubmed:meshHeading | pubmed-meshheading:15368281... | lld:pubmed |
| pubmed-article:15368281 | pubmed:meshHeading | pubmed-meshheading:15368281... | lld:pubmed |
| pubmed-article:15368281 | pubmed:meshHeading | pubmed-meshheading:15368281... | lld:pubmed |
| pubmed-article:15368281 | pubmed:meshHeading | pubmed-meshheading:15368281... | lld:pubmed |
| pubmed-article:15368281 | pubmed:meshHeading | pubmed-meshheading:15368281... | lld:pubmed |
| pubmed-article:15368281 | pubmed:meshHeading | pubmed-meshheading:15368281... | lld:pubmed |
| pubmed-article:15368281 | pubmed:meshHeading | pubmed-meshheading:15368281... | lld:pubmed |
| pubmed-article:15368281 | pubmed:year | 2004 | lld:pubmed |
| pubmed-article:15368281 | pubmed:articleTitle | Self-peptides that bind with low affinity to the diabetes-associated I-A(g7) molecule readily induce T cell tolerance in non-obese diabetic mice. | lld:pubmed |
| pubmed-article:15368281 | pubmed:affiliation | INSERM E0344, Université de Nice-Sophia Antipolis, Valbonne, France. | lld:pubmed |
| pubmed-article:15368281 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:15368281 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| entrez-gene:269846 | entrezgene:pubmed | pubmed-article:15368281 | lld:entrezgene |
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