Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
1
pubmed:dateCreated
2005-3-8
pubmed:abstractText
HIV has evolved several strategies to evade recognition by the host immune system including down-regulation of major histocompatibility complex (MHC) class I molecules. However, reduced expression of MHC class I molecules may stimulate natural killer (NK) cell lysis in cells of haematopoietic lineage. Here, we describe how HIV counteracts stimulation of NK cells by stabilizing surface expression of the non-classical MHC class I molecule, HLA-E. We demonstrate enhanced expression of HLA-E on lymphocytes from HIV-infected patients and show that in vitro infection of lymphocytes with HIV results in up-regulation of HLA-E expression and reduced susceptibility to NK cell cytotoxicity. Using HLA-E transfected K-562 cells, we identified the well-known HIV T-cell epitope p24 aa14-22a as a ligand for HLA-E that stabilizes surface expression of HLA-E, favouring inhibition of NK cell cytotoxicity. These results propose HIV-mediated up-regulation of HLA-E expression as an additional evasion strategy targeting the antiviral activities of NK cells, which may contribute to the capability of the virus in establishing chronic infection.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
http://linkedlifedata.com/resource/pubmed/chemical/ATP-Binding Cassette Transporters, http://linkedlifedata.com/resource/pubmed/chemical/Antigens, CD, http://linkedlifedata.com/resource/pubmed/chemical/DNA, http://linkedlifedata.com/resource/pubmed/chemical/Epitopes, http://linkedlifedata.com/resource/pubmed/chemical/HIV Core Protein p24, http://linkedlifedata.com/resource/pubmed/chemical/HLA Antigens, http://linkedlifedata.com/resource/pubmed/chemical/HLA-E antigen, http://linkedlifedata.com/resource/pubmed/chemical/Histocompatibility Antigens Class I, http://linkedlifedata.com/resource/pubmed/chemical/Lectins, C-Type, http://linkedlifedata.com/resource/pubmed/chemical/Ligands, http://linkedlifedata.com/resource/pubmed/chemical/NK Cell Lectin-Like Receptor..., http://linkedlifedata.com/resource/pubmed/chemical/RNA, Messenger, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Immunologic, http://linkedlifedata.com/resource/pubmed/chemical/Receptors, Natural Killer Cell, http://linkedlifedata.com/resource/pubmed/chemical/TAP1 protein, human, http://linkedlifedata.com/resource/pubmed/chemical/TAP2 protein, human
pubmed:status
MEDLINE
pubmed:issn
1359-6535
pubmed:author
pubmed:issnType
Print
pubmed:volume
10
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
95-107
pubmed:dateRevised
2008-11-21
pubmed:meshHeading
pubmed-meshheading:15751767-ATP-Binding Cassette Transporters, pubmed-meshheading:15751767-Amino Acid Sequence, pubmed-meshheading:15751767-Antigens, CD, pubmed-meshheading:15751767-Base Sequence, pubmed-meshheading:15751767-CD4-Positive T-Lymphocytes, pubmed-meshheading:15751767-Case-Control Studies, pubmed-meshheading:15751767-Cytotoxicity, Immunologic, pubmed-meshheading:15751767-DNA, pubmed-meshheading:15751767-Epitopes, pubmed-meshheading:15751767-HIV Core Protein p24, pubmed-meshheading:15751767-HIV Infections, pubmed-meshheading:15751767-HIV-1, pubmed-meshheading:15751767-HLA Antigens, pubmed-meshheading:15751767-Histocompatibility Antigens Class I, pubmed-meshheading:15751767-Humans, pubmed-meshheading:15751767-K562 Cells, pubmed-meshheading:15751767-Killer Cells, Natural, pubmed-meshheading:15751767-Lectins, C-Type, pubmed-meshheading:15751767-Ligands, pubmed-meshheading:15751767-Molecular Sequence Data, pubmed-meshheading:15751767-NK Cell Lectin-Like Receptor Subfamily D, pubmed-meshheading:15751767-RNA, Messenger, pubmed-meshheading:15751767-Receptors, Immunologic, pubmed-meshheading:15751767-Receptors, Natural Killer Cell, pubmed-meshheading:15751767-Transfection, pubmed-meshheading:15751767-Up-Regulation
pubmed:year
2005
pubmed:articleTitle
HIV-1 infection leads to increased HLA-E expression resulting in impaired function of natural killer cells.
pubmed:affiliation
Department of Internal Medicine I, Rheinische Friedrich-Wilhelms-Universität, Bonn, Germany. Jacob.Nattermann@ukb.uni-bonn.de
pubmed:publicationType
Journal Article, In Vitro, Research Support, Non-U.S. Gov't