|
rdf:type |
|
|
lifeskim:mentions |
umls-concept:C0001721,
umls-concept:C0017431,
umls-concept:C0021311,
umls-concept:C0030956,
umls-concept:C0039194,
umls-concept:C0085358,
umls-concept:C0086418,
umls-concept:C0205296,
umls-concept:C0220847,
umls-concept:C0332281,
umls-concept:C0524637,
umls-concept:C0750729,
umls-concept:C1332717,
umls-concept:C1413244,
umls-concept:C1415585,
umls-concept:C1706438,
umls-concept:C2698600
|
|
pubmed:issue |
9
|
|
pubmed:dateCreated |
2009-10-12
|
|
pubmed:abstractText |
Recently, we showed chronic hepatitis C to be associated with increased expression of HLA-E and identified peptide hepatitis C virus (HCV) core amino acids 35-44 as a ligand for HLA-E that stabilizes HLA-E expression, favoring inhibition of natural killer cell cytotoxicity. Here we describe HLA-E-restricted recognition of peptide HCV core amino acids 35-44 by CD8(+) T cells. Frequency of HLA-E-restricted responses was significantly higher in patients homozygous for the HLA-E(R) allele (60% vs 38%; P = .038). Moreover, we found that the HLA-E(R) allelic variant confers protection against chronic infection with HCV genotypes 2 and 3. Taken together, our data indicate an important immunomodulating function of HLA-E in hepatitis C.
|
|
pubmed:language |
eng
|
|
pubmed:journal |
|
|
pubmed:citationSubset |
AIM
|
|
pubmed:chemical |
|
|
pubmed:status |
MEDLINE
|
|
pubmed:month |
Nov
|
|
pubmed:issn |
1537-6613
|
|
pubmed:author |
pubmed-author:BergThomasT,
pubmed-author:KörnerChristianC,
pubmed-author:KrämerBenjaminB,
pubmed-author:LanghansBettinaB,
pubmed-author:MichalkMonikaM,
pubmed-author:NattermannJacobJ,
pubmed-author:NischalkeHans DieterHD,
pubmed-author:RockstrohJürgen KJK,
pubmed-author:SauerbruchTilmanT,
pubmed-author:SchulteDanielaD,
pubmed-author:SpenglerUlrichU,
pubmed-author:SteinbergVerenaV,
pubmed-author:VogelMartinM
|
|
pubmed:issnType |
Electronic
|
|
pubmed:day |
1
|
|
pubmed:volume |
200
|
|
pubmed:owner |
NLM
|
|
pubmed:authorsComplete |
Y
|
|
pubmed:pagination |
1397-401
|
|
pubmed:dateRevised |
2010-1-26
|
|
pubmed:meshHeading |
pubmed-meshheading:19780673-Adult,
pubmed-meshheading:19780673-Aged,
pubmed-meshheading:19780673-Aged, 80 and over,
pubmed-meshheading:19780673-CD8-Positive T-Lymphocytes,
pubmed-meshheading:19780673-Case-Control Studies,
pubmed-meshheading:19780673-Female,
pubmed-meshheading:19780673-HLA Antigens,
pubmed-meshheading:19780673-Hepacivirus,
pubmed-meshheading:19780673-Hepatitis C, Chronic,
pubmed-meshheading:19780673-Histocompatibility Antigens Class I,
pubmed-meshheading:19780673-Humans,
pubmed-meshheading:19780673-Interferon-gamma,
pubmed-meshheading:19780673-Male,
pubmed-meshheading:19780673-Middle Aged,
pubmed-meshheading:19780673-Viral Load,
pubmed-meshheading:19780673-Young Adult
|
|
pubmed:year |
2009
|
|
pubmed:articleTitle |
The HLA-E(R)/HLA-E(R) genotype affects the natural course of hepatitis C virus (HCV) infection and is associated with HLA-E-restricted recognition of an HCV-derived peptide by interferon-gamma-secreting human CD8(+) T cells.
|
|
pubmed:affiliation |
Department of Internal Medicine I, University of Bonn, Bonn, Germany.
|
|
pubmed:publicationType |
Journal Article,
Research Support, Non-U.S. Gov't
|
