pubmed-article:20037585 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20037585 | lifeskim:mentions | umls-concept:C0111208 | lld:lifeskim |
pubmed-article:20037585 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:20037585 | lifeskim:mentions | umls-concept:C1136169 | lld:lifeskim |
pubmed-article:20037585 | lifeskim:mentions | umls-concept:C0036588 | lld:lifeskim |
pubmed-article:20037585 | lifeskim:mentions | umls-concept:C0441712 | lld:lifeskim |
pubmed-article:20037585 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:20037585 | pubmed:dateCreated | 2010-1-19 | lld:pubmed |
pubmed-article:20037585 | pubmed:abstractText | The inhibitory immunoregulatory receptor CTLA-4 is critical in maintaining self-tolerance, but the mechanisms of its actions have remained controversial. Here we examined the antigen specificity of tissue-infiltrating CD4(+) T cells in Ctla4(-/-) mice. After adoptive transfer, T cells isolated from tissues of Ctla4(-/-) mice showed T cell antigen receptor (TCR)-dependent accumulation in the tissues from which they were derived, which suggested reactivity to tissue-specific antigens. We identified the pancreas-specific enzyme PDIA2 as an autoantigen in Ctla4(-/-) mice. CTLA-4 expressed either on PDIA2-specific effector cells or on regulatory T cells was sufficient to control tissue destruction mediated by PDIA2-specific T cells. Our results demonstrate that both cell-intrinsic and non-cell-autonomous actions of CTLA-4 operate to maintain T cell tolerance to a self antigen. | lld:pubmed |
pubmed-article:20037585 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20037585 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20037585 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20037585 | pubmed:language | eng | lld:pubmed |
pubmed-article:20037585 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20037585 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:20037585 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20037585 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20037585 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20037585 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20037585 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20037585 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20037585 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20037585 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:20037585 | pubmed:month | Feb | lld:pubmed |
pubmed-article:20037585 | pubmed:issn | 1529-2916 | lld:pubmed |
pubmed-article:20037585 | pubmed:author | pubmed-author:KohyamaMasako... | lld:pubmed |
pubmed-article:20037585 | pubmed:author | pubmed-author:SuriAnishA | lld:pubmed |
pubmed-article:20037585 | pubmed:author | pubmed-author:UnanueEmil... | lld:pubmed |
pubmed-article:20037585 | pubmed:author | pubmed-author:MurphyKenneth... | lld:pubmed |
pubmed-article:20037585 | pubmed:author | pubmed-author:IseWataruW | lld:pubmed |
pubmed-article:20037585 | pubmed:author | pubmed-author:MurphyTheresa... | lld:pubmed |
pubmed-article:20037585 | pubmed:author | pubmed-author:LeeHyang MiHM | lld:pubmed |
pubmed-article:20037585 | pubmed:author | pubmed-author:NutschKatheri... | lld:pubmed |
pubmed-article:20037585 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:20037585 | pubmed:volume | 11 | lld:pubmed |
pubmed-article:20037585 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:20037585 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:20037585 | pubmed:pagination | 129-35 | lld:pubmed |
pubmed-article:20037585 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
pubmed-article:20037585 | pubmed:meshHeading | pubmed-meshheading:20037585... | lld:pubmed |
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pubmed-article:20037585 | pubmed:meshHeading | pubmed-meshheading:20037585... | lld:pubmed |
pubmed-article:20037585 | pubmed:meshHeading | pubmed-meshheading:20037585... | lld:pubmed |
pubmed-article:20037585 | pubmed:meshHeading | pubmed-meshheading:20037585... | lld:pubmed |
pubmed-article:20037585 | pubmed:meshHeading | pubmed-meshheading:20037585... | lld:pubmed |
pubmed-article:20037585 | pubmed:year | 2010 | lld:pubmed |
pubmed-article:20037585 | pubmed:articleTitle | CTLA-4 suppresses the pathogenicity of self antigen-specific T cells by cell-intrinsic and cell-extrinsic mechanisms. | lld:pubmed |
pubmed-article:20037585 | pubmed:affiliation | Department of Pathology and Immunology, Washington University School of Medicine, St. Louis, Missouri, USA. | lld:pubmed |
pubmed-article:20037585 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:20037585 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
pubmed-article:20037585 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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