| pubmed-article:16956940 | rdf:type | pubmed:Citation | lld:pubmed |
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| pubmed-article:16956940 | lifeskim:mentions | umls-concept:C0400914 | lld:lifeskim |
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| pubmed-article:16956940 | lifeskim:mentions | umls-concept:C1413244 | lld:lifeskim |
| pubmed-article:16956940 | lifeskim:mentions | umls-concept:C2698600 | lld:lifeskim |
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| pubmed-article:16956940 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
| pubmed-article:16956940 | pubmed:issue | 22 | lld:pubmed |
| pubmed-article:16956940 | pubmed:dateCreated | 2006-10-30 | lld:pubmed |
| pubmed-article:16956940 | pubmed:abstractText | Hepatitis C virus (HCV)-specific CD8 cell exhaustion may represent a mechanism of HCV persistence. The inhibitory receptor PD-1 has been reported to be up-regulated in exhausted CD8 cells. Therefore, we studied PD-1 expression longitudinally during acute HCV infection. Most HCV-specific CD8 cells expressed PD-1 at the time of acute illness, irrespective of the final outcome. PD-1 expression declined with the acquisition of a memory phenotype and recovery of an efficient CD8 cell function in resolving HCV infections, whereas high levels were maintained when HCV persisted and HCV-specific CD8 cells remained dysfunctional. Blocking PD-1/PDL-1 interaction with an anti-PDL-1 antibody improved the capacity of expansion of virus-specific CD8 cells. | lld:pubmed |
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| pubmed-article:16956940 | pubmed:language | eng | lld:pubmed |
| pubmed-article:16956940 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:16956940 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:16956940 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:16956940 | pubmed:month | Nov | lld:pubmed |
| pubmed-article:16956940 | pubmed:issn | 0022-538X | lld:pubmed |
| pubmed-article:16956940 | pubmed:author | pubmed-author:MassariMarcoM | lld:pubmed |
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| pubmed-article:16956940 | pubmed:author | pubmed-author:UrbaniSimonaS | lld:pubmed |
| pubmed-article:16956940 | pubmed:author | pubmed-author:AmadeiBarbara... | lld:pubmed |
| pubmed-article:16956940 | pubmed:author | pubmed-author:SchivazappaSi... | lld:pubmed |
| pubmed-article:16956940 | pubmed:author | pubmed-author:TolaDanielaD | lld:pubmed |
| pubmed-article:16956940 | pubmed:issnType | Print | lld:pubmed |
| pubmed-article:16956940 | pubmed:volume | 80 | lld:pubmed |
| pubmed-article:16956940 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:16956940 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:16956940 | pubmed:pagination | 11398-403 | lld:pubmed |
| pubmed-article:16956940 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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| pubmed-article:16956940 | pubmed:year | 2006 | lld:pubmed |
| pubmed-article:16956940 | pubmed:articleTitle | PD-1 expression in acute hepatitis C virus (HCV) infection is associated with HCV-specific CD8 exhaustion. | lld:pubmed |
| pubmed-article:16956940 | pubmed:affiliation | Laboratorio Immunopatologia Virale, Unit of Infectious Diseases and Hepatology, Azienda Ospedaliero-Universitaria di Parma, Via Gramsci 14, 43100 Parma, Italy. | lld:pubmed |
| pubmed-article:16956940 | pubmed:publicationType | Journal Article | lld:pubmed |
| pubmed-article:16956940 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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