rdf:type |
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lifeskim:mentions |
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pubmed:issue |
1
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pubmed:dateCreated |
2007-12-24
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pubmed:abstractText |
B7-H1 (also known as CD274 and PD-L1) is a cosignalling molecule regulating T-cell immunity positively or negatively in vivo. However, little is known about the role of endogenous B7-H1 in bacterial infection. We found that B7-H1 expression was up-regulated in various cell populations including CD4+ and CD8+ T cells, natural killer (NK) cells and macrophages following Listeria monocytogenes infection. Administration of the antagonistic B7-H1 monoclonal antibody resulted in a significant increase in mortality in mice infected with a lethal dose of L. monocytogenes compared with mice given the control immunoglobulin. In vivo blockade of B7-H1 greatly inhibited the production of tumour necrosis factor (TNF)-alpha and nitric oxide, key effector molecules responsible for intracellular killing by macrophages. B7-H1 blockade also suppressed the expression of granzyme B and interferon (IFN)-gamma by NK cells. Interestingly, blocking of endogenous B7-H1 selectively inhibited CD8+ T cells rather than CD4+ T cells in response to L. monocytogenes infection, as evidenced by the reduction of IFN-gamma production and the expression of effector surface markers including CD62L(int/low) and CD44(high) in CD8+ T cells from mice given anti-B7-H1 monoclonal antibody. In addition, we found that the proliferation of listeriolysin-O (LLO)-specific and IFN-gamma-producing L. monocytogenes-reactive CD8+ T cells was significantly decreased not only in the effector phase but also in the memory phase in the presence of anti-B7-H1 antibody. Our findings thus suggest that endogenous B7-H1 can provide positive costimulatory signals for innate and adaptive immunity leading to protection against intracellular bacterial infection.
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/17971153-10023768,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/17971153-9143691
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Jan
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pubmed:issn |
1365-2567
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:volume |
123
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
90-9
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pubmed:dateRevised |
2011-11-17
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pubmed:meshHeading |
pubmed-meshheading:17971153-Animals,
pubmed-meshheading:17971153-Mice,
pubmed-meshheading:17971153-Peptides,
pubmed-meshheading:17971153-Listeriosis,
pubmed-meshheading:17971153-Immune Tolerance,
pubmed-meshheading:17971153-Colony Count, Microbial,
pubmed-meshheading:17971153-Lymphocyte Activation,
pubmed-meshheading:17971153-Mice, Inbred BALB C,
pubmed-meshheading:17971153-Immunity, Cellular,
pubmed-meshheading:17971153-Mice, Inbred C57BL,
pubmed-meshheading:17971153-Immunity, Innate,
pubmed-meshheading:17971153-Cell Proliferation,
pubmed-meshheading:17971153-Antibodies, Monoclonal,
pubmed-meshheading:17971153-Membrane Glycoproteins,
pubmed-meshheading:17971153-Up-Regulation,
pubmed-meshheading:17971153-CD8-Positive T-Lymphocytes,
pubmed-meshheading:17971153-Antigens, CD80,
pubmed-meshheading:17971153-Antigens, CD274
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