Linked Life Data

17405908

Source:http://linkedlifedata.com/resource/pubmed/id/17405908

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
2
pubmed:dateCreated
2007-7-3
pubmed:abstractText
Recent evidence indicates that natural killer (NK) cells can negatively regulate T-cell responses, but the mechanisms behind this phenomenon as a consequence of NK-T-cell interactions are poorly understood. We studied the interaction between the NKG2D receptor and its ligands (NKG2DLs), and asked whether T cells expressed NKG2DLs in response to superantigen, alloantigen, or a specific antigenic peptide, and if this rendered them susceptible to NK lysis. As evaluated by FACS, the major histocompatibility complex (MHC) class I chain-related protein A (MICA) was the ligand expressed earlier on both CD4(+) and CD8(+) T cells in 90% of the donors tested, while UL16-binding protein-1 (ULBP)1, ULBP2, and ULBP3 were induced at later times in 55%-75% of the donors. By carboxyfluorescein diacetate succinimidyl ester (CFSE) labeling, we observed that NKG2DLs were expressed mainly on T cells that had gone through at least one division. Real-time reverse-transcription polymerase chain reaction confirmed the expression of all NKG2DLs, except ULBP4. In addition, T-cell activation stimulated phosphorylation of ataxia-telangiectasia mutated (ATM), a kinase required for NKG2DLs expression after DNA damage, and ATM/Rad3-related kinase (ATR) inhibitors blocked MICA induction on T cells with a mechanism involving NF-kappaB. Finally, we demonstrated that activated T cells became susceptible to autologous NK lysis via NKG2D/NKG2DLs interaction and granule exocytosis, suggesting that NK lysis of T lymphocytes via NKG2D may be an additional mechanism to limit T-cell responses.
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
AIM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Jul
pubmed:issn
0006-4971
pubmed:author
pubmed:issnType
Print
pubmed:day
15
pubmed:volume
110
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
606-15
pubmed:dateRevised
2010-11-18
pubmed:meshHeading
pubmed-meshheading:17405908-Autolysis, pubmed-meshheading:17405908-CD4-Positive T-Lymphocytes, pubmed-meshheading:17405908-CD8-Positive T-Lymphocytes, pubmed-meshheading:17405908-Cell Survival, pubmed-meshheading:17405908-Flow Cytometry, pubmed-meshheading:17405908-GPI-Linked Proteins, pubmed-meshheading:17405908-Gene Expression Regulation, pubmed-meshheading:17405908-Histocompatibility Antigens Class I, pubmed-meshheading:17405908-Humans, pubmed-meshheading:17405908-Intercellular Signaling Peptides and Proteins, pubmed-meshheading:17405908-Isoantigens, pubmed-meshheading:17405908-Killer Cells, Natural, pubmed-meshheading:17405908-Leukocytes, Mononuclear, pubmed-meshheading:17405908-Lymphocyte Activation, pubmed-meshheading:17405908-NF-kappa B, pubmed-meshheading:17405908-Polymerase Chain Reaction, pubmed-meshheading:17405908-RNA, pubmed-meshheading:17405908-T-Lymphocytes
pubmed:year
2007
pubmed:articleTitle
Antigen-activated human T lymphocytes express cell-surface NKG2D ligands via an ATM/ATR-dependent mechanism and become susceptible to autologous NK- cell lysis.
pubmed:affiliation
Department of Experimental Medicine, Istituto Pasteur-Fondazione Cenci Bolognetti, University La Sapienza, Rome, Italy.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't