pubmed-article:19332785 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:19332785 | lifeskim:mentions | umls-concept:C0035820 | lld:lifeskim |
pubmed-article:19332785 | lifeskim:mentions | umls-concept:C0599840 | lld:lifeskim |
pubmed-article:19332785 | lifeskim:mentions | umls-concept:C0024432 | lld:lifeskim |
pubmed-article:19332785 | lifeskim:mentions | umls-concept:C0243026 | lld:lifeskim |
pubmed-article:19332785 | lifeskim:mentions | umls-concept:C0032214 | lld:lifeskim |
pubmed-article:19332785 | lifeskim:mentions | umls-concept:C0600138 | lld:lifeskim |
pubmed-article:19332785 | lifeskim:mentions | umls-concept:C1155266 | lld:lifeskim |
pubmed-article:19332785 | lifeskim:mentions | umls-concept:C0017262 | lld:lifeskim |
pubmed-article:19332785 | lifeskim:mentions | umls-concept:C1521733 | lld:lifeskim |
pubmed-article:19332785 | lifeskim:mentions | umls-concept:C0449297 | lld:lifeskim |
pubmed-article:19332785 | lifeskim:mentions | umls-concept:C2911684 | lld:lifeskim |
pubmed-article:19332785 | lifeskim:mentions | umls-concept:C0185117 | lld:lifeskim |
pubmed-article:19332785 | pubmed:issue | 15 | lld:pubmed |
pubmed-article:19332785 | pubmed:dateCreated | 2009-4-16 | lld:pubmed |
pubmed-article:19332785 | pubmed:abstractText | Sepsis, a leading cause of death worldwide, involves concomitant expression of an overzealous inflammatory response and inefficient bacterial clearance. Macrophage function is pivotal to the development of these two aspects during sepsis; however, the mechanisms underlying these changes remain unclear. Here we report that the PD-1:PD-L pathway appears to be a determining factor of the outcome of sepsis, regulating the delicate balance between effectiveness and damage by the antimicrobial immune response. To this end we observed that PD-1(-/-) mice were markedly protected from the lethality of sepsis, accompanied by a decreased bacterial burden and suppressed inflammatory cytokine response. To the extent that this is a macrophage-specific aspect of the effects of PD-1, we found the following: first, peritoneal macrophages expressed significantly higher levels of PD-1 during sepsis, which was associated with their development of cellular dysfunction; second, when peritoneal macrophages were depleted (using clodronate liposomes) from PD-1(-/-) mice, the animals' bactericidal capacity was lowered, their inflammatory cytokine levels were elevated, and protection from septic lethality was diminished; and third, blood monocytes from both septic mice and patients with septic shock shared markedly increased PD-1 levels. Together, these data suggest that PD-1 may not only be a dysfunctional marker/effector of macrophages/monocytes, but may also be a potential therapeutic target for designing measures to modulate the innate immune response, thereby preventing the detrimental effects of sepsis. | lld:pubmed |
pubmed-article:19332785 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19332785 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19332785 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19332785 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19332785 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19332785 | pubmed:grant | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:19332785 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19332785 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:19332785 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:19332785 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19332785 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19332785 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19332785 | pubmed:commentsCorrections | http://linkedlifedata.com/r... | lld:pubmed |
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pubmed-article:19332785 | pubmed:language | eng | lld:pubmed |
pubmed-article:19332785 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19332785 | pubmed:citationSubset | IM | lld:pubmed |
pubmed-article:19332785 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19332785 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19332785 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19332785 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19332785 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19332785 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19332785 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19332785 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:19332785 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:19332785 | pubmed:month | Apr | lld:pubmed |
pubmed-article:19332785 | pubmed:issn | 1091-6490 | lld:pubmed |
pubmed-article:19332785 | pubmed:author | pubmed-author:MonneretGuill... | lld:pubmed |
pubmed-article:19332785 | pubmed:author | pubmed-author:AyalaAlfredA | lld:pubmed |
pubmed-article:19332785 | pubmed:author | pubmed-author:ChungChun-Shi... | lld:pubmed |
pubmed-article:19332785 | pubmed:author | pubmed-author:HuangXinX | lld:pubmed |
pubmed-article:19332785 | pubmed:author | pubmed-author:LepapeAlainA | lld:pubmed |
pubmed-article:19332785 | pubmed:author | pubmed-author:ChenYapingY | lld:pubmed |
pubmed-article:19332785 | pubmed:author | pubmed-author:YuanZhenglong... | lld:pubmed |
pubmed-article:19332785 | pubmed:author | pubmed-author:VenetFabienne... | lld:pubmed |
pubmed-article:19332785 | pubmed:author | pubmed-author:SwanRyanR | lld:pubmed |
pubmed-article:19332785 | pubmed:author | pubmed-author:WangYvonne... | lld:pubmed |
pubmed-article:19332785 | pubmed:author | pubmed-author:KheroufHakimH | lld:pubmed |
pubmed-article:19332785 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:19332785 | pubmed:day | 14 | lld:pubmed |
pubmed-article:19332785 | pubmed:volume | 106 | lld:pubmed |
pubmed-article:19332785 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:19332785 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:19332785 | pubmed:pagination | 6303-8 | lld:pubmed |
pubmed-article:19332785 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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pubmed-article:19332785 | pubmed:year | 2009 | lld:pubmed |
pubmed-article:19332785 | pubmed:articleTitle | PD-1 expression by macrophages plays a pathologic role in altering microbial clearance and the innate inflammatory response to sepsis. | lld:pubmed |