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rdf:type |
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lifeskim:mentions |
umls-concept:C0017262,
umls-concept:C0152060,
umls-concept:C0185117,
umls-concept:C0205154,
umls-concept:C0205217,
umls-concept:C0220847,
umls-concept:C0231174,
umls-concept:C0280274,
umls-concept:C0524910,
umls-concept:C0681842,
umls-concept:C0871261,
umls-concept:C1306235,
umls-concept:C1704632,
umls-concept:C1705241,
umls-concept:C1705242,
umls-concept:C1706817,
umls-concept:C2728259,
umls-concept:C2911684,
umls-concept:C2911692
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pubmed:issue |
6
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pubmed:dateCreated |
2008-3-6
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pubmed:abstractText |
Up-regulation of programmed death-1 (PD-1) identifies exhausted T cells in various mouse and human viral models including chronic hepatitis C virus (HCV) infection, which is characterized by impaired CTL function. A large proportion of patients fail to eradicate HCV with current IFN-based antiviral therapy; in particular, African Americans are less likely to respond, but the mechanisms for these differences are not fully elucidated. In this study, in 72 treatment-naive patients with persistent HCV we found that PD-1 was significantly up-regulated on CD4(+) and CD8(+) T cells, HCV-specific CTLs, and NK cells. Increased PD-1 on HCV-specific CTLs was significantly associated with failed early and sustained virologic response to therapy in African American but not Caucasian American patients. Patients with sustained virologic response showed decreases in PD-1 on total CD4(+) T cells, HCV-specific CTLs, and the CD56(bright) NK subset after therapy completion. Collectively, these data indicate that PD-1 is critical in persistent HCV and successful therapy results in global down-regulation of its expression.
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pubmed:grant |
http://linkedlifedata.com/resource/pubmed/grant/R01 DK071560,
http://linkedlifedata.com/resource/pubmed/grant/U01 DK60309,
http://linkedlifedata.com/resource/pubmed/grant/U01 DK60324,
http://linkedlifedata.com/resource/pubmed/grant/U01 DK60327,
http://linkedlifedata.com/resource/pubmed/grant/U01 DK60329,
http://linkedlifedata.com/resource/pubmed/grant/U01 DK60335,
http://linkedlifedata.com/resource/pubmed/grant/U01 DK60340,
http://linkedlifedata.com/resource/pubmed/grant/U01 DK60341,
http://linkedlifedata.com/resource/pubmed/grant/U01 DK60342,
http://linkedlifedata.com/resource/pubmed/grant/U01 DK60344,
http://linkedlifedata.com/resource/pubmed/grant/U01 DK60345,
http://linkedlifedata.com/resource/pubmed/grant/U01 DK60346,
http://linkedlifedata.com/resource/pubmed/grant/U01 DK60349,
http://linkedlifedata.com/resource/pubmed/grant/U01 DK60352
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
AIM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Mar
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pubmed:issn |
0022-1767
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pubmed:author |
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pubmed:issnType |
Print
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pubmed:day |
15
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pubmed:volume |
180
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
3637-41
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:18322167-African Americans,
pubmed-meshheading:18322167-Alleles,
pubmed-meshheading:18322167-Antigens, CD,
pubmed-meshheading:18322167-Antiviral Agents,
pubmed-meshheading:18322167-Apoptosis Regulatory Proteins,
pubmed-meshheading:18322167-European Continental Ancestry Group,
pubmed-meshheading:18322167-Female,
pubmed-meshheading:18322167-Genotype,
pubmed-meshheading:18322167-HLA Antigens,
pubmed-meshheading:18322167-Hepacivirus,
pubmed-meshheading:18322167-Hepatitis C, Chronic,
pubmed-meshheading:18322167-Humans,
pubmed-meshheading:18322167-Male,
pubmed-meshheading:18322167-Middle Aged,
pubmed-meshheading:18322167-Predictive Value of Tests,
pubmed-meshheading:18322167-Programmed Cell Death 1 Receptor,
pubmed-meshheading:18322167-T-Lymphocyte Subsets,
pubmed-meshheading:18322167-Up-Regulation
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pubmed:year |
2008
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pubmed:articleTitle |
Cutting edge: programmed death-1 expression is increased on immunocytes in chronic hepatitis C virus and predicts failure of response to antiviral therapy: race-dependent differences.
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pubmed:affiliation |
Division of Gastroenterology and Hepatology, Hepatitis C Center, University of Colorado Health Sciences Center and National Jewish Hospital, Aurora, Co 80045, USA.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't,
Research Support, N.I.H., Extramural,
Research Support, N.I.H., Intramural
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