pubmed-article:18566376 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:18566376 | lifeskim:mentions | umls-concept:C0041296 | lld:lifeskim |
pubmed-article:18566376 | lifeskim:mentions | umls-concept:C0086418 | lld:lifeskim |
pubmed-article:18566376 | lifeskim:mentions | umls-concept:C0011065 | lld:lifeskim |
pubmed-article:18566376 | lifeskim:mentions | umls-concept:C0039194 | lld:lifeskim |
pubmed-article:18566376 | lifeskim:mentions | umls-concept:C0542341 | lld:lifeskim |
pubmed-article:18566376 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
pubmed-article:18566376 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
pubmed-article:18566376 | lifeskim:mentions | umls-concept:C2728259 | lld:lifeskim |
pubmed-article:18566376 | pubmed:issue | 1 | lld:pubmed |
pubmed-article:18566376 | pubmed:dateCreated | 2008-6-20 | lld:pubmed |
pubmed-article:18566376 | pubmed:abstractText | Protective immunity against Mycobacterium tuberculosis requires the generation of cell-mediated immunity. We investigated the expression and role of programmed death 1 (PD-1) and its ligands, molecules known to modulate T cell activation, in the regulation of IFN-gamma production and lytic degranulation during human tuberculosis. We demonstrated that specific Ag-stimulation increased CD3+PD-1+ lymphocytes in peripheral blood and pleural fluid from tuberculosis patients in direct correlation with IFN-gamma production from these individuals. Moreover, M. tuberculosis-induced IFN-gamma participated in the up-regulation of PD-1 expression. Blockage of PD-1 or PD-1 and its ligands (PD-Ls: PD-L1, PD-L2) enhanced the specific degranulation of CD8+ T cells and the percentage of specific IFN-gamma-producing lymphocytes against the pathogen, demonstrating that the PD-1:PD-Ls pathway inhibits T cell effector functions during active M. tuberculosis infection. Furthermore, the simultaneous blockage of the inhibitory receptor PD-1 together with the activation of the costimulatory protein signaling lymphocytic activation molecule led to the promotion of protective IFN-gamma responses to M. tuberculosis, even in patients with weak cell-mediated immunity against the bacteria. Together, we demonstrated that PD-1 interferes with T cell effector functions against M. tuberculosis, suggesting that PD-1 has a key regulatory role during the immune response of the host to the pathogen. | lld:pubmed |
pubmed-article:18566376 | pubmed:language | eng | lld:pubmed |
pubmed-article:18566376 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:18566376 | pubmed:citationSubset | AIM | lld:pubmed |
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pubmed-article:18566376 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:18566376 | pubmed:month | Jul | lld:pubmed |
pubmed-article:18566376 | pubmed:issn | 0022-1767 | lld:pubmed |
pubmed-article:18566376 | pubmed:author | pubmed-author:ChuluyanH... | lld:pubmed |
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pubmed-article:18566376 | pubmed:author | pubmed-author:MartínezGusta... | lld:pubmed |
pubmed-article:18566376 | pubmed:author | pubmed-author:MusellaRosa... | lld:pubmed |
pubmed-article:18566376 | pubmed:author | pubmed-author:JuradoJavier... | lld:pubmed |
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pubmed-article:18566376 | pubmed:issnType | Print | lld:pubmed |
pubmed-article:18566376 | pubmed:day | 1 | lld:pubmed |
pubmed-article:18566376 | pubmed:volume | 181 | lld:pubmed |
pubmed-article:18566376 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:18566376 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:18566376 | pubmed:pagination | 116-25 | lld:pubmed |
pubmed-article:18566376 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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pubmed-article:18566376 | pubmed:year | 2008 | lld:pubmed |
pubmed-article:18566376 | pubmed:articleTitle | Programmed death (PD)-1:PD-ligand 1/PD-ligand 2 pathway inhibits T cell effector functions during human tuberculosis. | lld:pubmed |
pubmed-article:18566376 | pubmed:affiliation | Department of Biological Chemistry, School of Sciences, University of Buenos Aires, Buenos Aires, Argentina. | lld:pubmed |
pubmed-article:18566376 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:18566376 | pubmed:publicationType | Research Support, Non-U.S. Gov't | lld:pubmed |
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