Linked Life Data

16917489

Source:http://linkedlifedata.com/resource/pubmed/id/16917489

Statements in which the resource exists as a subject.
PredicateObject
rdf:type
lifeskim:mentions
pubmed:issue
10
pubmed:dateCreated
2006-10-25
pubmed:abstractText
The engagement of programmed death 1 (PD-1) to its ligands, PD-L1 and PD-L2, inhibits proliferation and cytokine production mediated by antibodies to CD3 (refs. 5,6,7). Blocking the PD-1-PD-L1 pathway in mice chronically infected with lymphocytic choriomeningitis virus restores the capacity of exhausted CD8(+) T cells to undergo proliferation, cytokine production and cytotoxic activity and, consequently, results in reduced viral load. During chronic HIV infection, HIV-specific CD8(+) T cells are functionally impaired, showing a reduced capacity to produce cytokines and effector molecules as well as an impaired capacity to proliferate. Here, we found that PD-1 was upregulated on HIV-specific CD8(+) T cells; PD-1 expression levels were significantly correlated both with viral load and with the reduced capacity for cytokine production and proliferation of HIV-specific CD8(+) T cells. Notably, cytomegalovirus (CMV)-specific CD8(+) T cells from the same donors did not upregulate PD-1 and maintained the production of high levels of cytokines. Blocking PD-1 engagement to its ligand (PD-L1) enhanced the capacity of HIV-specific CD8(+) T cells to survive and proliferate and led to an increased production of cytokines and cytotoxic molecules in response to cognate antigen. The accumulation of HIV-specific dysfunctional CD8(+) T cells in the infected host could prevent the renewal of a functionally competent HIV-specific CD8(+) repertoire.
pubmed:commentsCorrections
pubmed:language
eng
pubmed:journal
pubmed:citationSubset
IM
pubmed:chemical
pubmed:status
MEDLINE
pubmed:month
Oct
pubmed:issn
1078-8956
pubmed:author
pubmed:issnType
Print
pubmed:volume
12
pubmed:owner
NLM
pubmed:authorsComplete
Y
pubmed:pagination
1198-202
pubmed:dateRevised
2011-11-17
pubmed:meshHeading
pubmed-meshheading:16917489-Amino Acid Sequence, pubmed-meshheading:16917489-Antigens, CD, pubmed-meshheading:16917489-Antigens, CD3, pubmed-meshheading:16917489-Apoptosis Regulatory Proteins, pubmed-meshheading:16917489-CD8-Positive T-Lymphocytes, pubmed-meshheading:16917489-Cell Differentiation, pubmed-meshheading:16917489-Cell Proliferation, pubmed-meshheading:16917489-Cytokines, pubmed-meshheading:16917489-HIV Infections, pubmed-meshheading:16917489-Humans, pubmed-meshheading:16917489-Immune System, pubmed-meshheading:16917489-Immune System Diseases, pubmed-meshheading:16917489-Immunophenotyping, pubmed-meshheading:16917489-Molecular Sequence Data, pubmed-meshheading:16917489-Programmed Cell Death 1 Receptor, pubmed-meshheading:16917489-Receptors, Antigen, T-Cell, pubmed-meshheading:16917489-Up-Regulation
pubmed:year
2006
pubmed:articleTitle
Upregulation of PD-1 expression on HIV-specific CD8+ T cells leads to reversible immune dysfunction.
pubmed:affiliation
Laboratoire d'Immunologie, Centre de Recherche du Centre Hospitalier de l'Université de Montréal (CR-CHUM) Saint-Luc, 264 Rene Levesque Est, Montréal, Québec H2X1P1, Canada.
pubmed:publicationType
Journal Article, Research Support, Non-U.S. Gov't