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| pubmed-article:17142723 | lifeskim:mentions | umls-concept:C1619636 | lld:lifeskim |
| pubmed-article:17142723 | lifeskim:mentions | umls-concept:C1514873 | lld:lifeskim |
| pubmed-article:17142723 | lifeskim:mentions | umls-concept:C2728259 | lld:lifeskim |
| pubmed-article:17142723 | lifeskim:mentions | umls-concept:C0205154 | lld:lifeskim |
| pubmed-article:17142723 | pubmed:issue | 12 | lld:pubmed |
| pubmed-article:17142723 | pubmed:dateCreated | 2006-12-4 | lld:pubmed |
| pubmed-article:17142723 | pubmed:abstractText | Constitutive presentation of tissue Ags by dendritic cells results in tolerance of autoreactive CD8+ T cells; however, the underlying molecular mechanisms are not well understood. In this study we show that programmed death (PD)-1, an inhibitory receptor of the CD28 family, is required for tolerance induction of autoreactive CD8+ T cells. An antagonistic Ab against PD-1 provoked destructive autoimmune diabetes in RIP-mOVA mice expressing chicken OVA in the pancreatic islet cells, which received naive OVA-specific CD8+ OT-I cells. This effect was mediated by the PD ligand (PD-L) PD-L1 but not by PD-L2. An increased number of effector OT-I cells recovered from the pancreatic lymph nodes of anti-PD-L1-treated mice showed down-regulation of PD-1. Furthermore, the blockade of PD-1/PD-L1 interaction during the priming phase did not significantly affect OT-I cell division but enhanced its granzyme B, IFN-gamma, and IL-2 production. Thus, during the presentation of tissue Ags to CD8+ T cells, PD-1/PD-L1 interaction crucially controls the effector differentiation of autoreactive T cells to maintain self-tolerance. | lld:pubmed |
| pubmed-article:17142723 | pubmed:language | eng | lld:pubmed |
| pubmed-article:17142723 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:17142723 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:17142723 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:17142723 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:17142723 | pubmed:month | Dec | lld:pubmed |
| pubmed-article:17142723 | pubmed:issn | 0022-1767 | lld:pubmed |
| pubmed-article:17142723 | pubmed:author | pubmed-author:YagitaHideoH | lld:pubmed |
| pubmed-article:17142723 | pubmed:author | pubmed-author:DongChenC | lld:pubmed |
| pubmed-article:17142723 | pubmed:author | pubmed-author:WangYi-HongYH | lld:pubmed |
| pubmed-article:17142723 | pubmed:author | pubmed-author:Martin-Orozco... | lld:pubmed |
| pubmed-article:17142723 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:17142723 | pubmed:day | 15 | lld:pubmed |
| pubmed-article:17142723 | pubmed:volume | 177 | lld:pubmed |
| pubmed-article:17142723 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:17142723 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:17142723 | pubmed:pagination | 8291-5 | lld:pubmed |
| pubmed-article:17142723 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:17142723 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:17142723 | pubmed:articleTitle | Cutting Edge: Programmed death (PD) ligand-1/PD-1 interaction is required for CD8+ T cell tolerance to tissue antigens. | lld:pubmed |
| pubmed-article:17142723 | pubmed:affiliation | University of Texas M.D. Anderson Cancer Center, 7455 Fannin, Houston, TX 77030, USA. | lld:pubmed |
| pubmed-article:17142723 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:17142723 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
| pubmed-article:17142723 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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