| pubmed-article:18268348 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:18268348 | lifeskim:mentions | umls-concept:C0016832 | lld:lifeskim |
| pubmed-article:18268348 | lifeskim:mentions | umls-concept:C0319941 | lld:lifeskim |
| pubmed-article:18268348 | lifeskim:mentions | umls-concept:C1167395 | lld:lifeskim |
| pubmed-article:18268348 | lifeskim:mentions | umls-concept:C0001721 | lld:lifeskim |
| pubmed-article:18268348 | lifeskim:mentions | umls-concept:C1704259 | lld:lifeskim |
| pubmed-article:18268348 | lifeskim:mentions | umls-concept:C0683598 | lld:lifeskim |
| pubmed-article:18268348 | lifeskim:mentions | umls-concept:C1705987 | lld:lifeskim |
| pubmed-article:18268348 | lifeskim:mentions | umls-concept:C0450254 | lld:lifeskim |
| pubmed-article:18268348 | pubmed:issue | 7 | lld:pubmed |
| pubmed-article:18268348 | pubmed:dateCreated | 2008-2-21 | lld:pubmed |
| pubmed-article:18268348 | pubmed:abstractText | The PD-1 costimulatory receptor inhibits T cell receptor signaling upon interacting with its ligands PD-L1 and PD-L2. The PD-1/PD-L pathway is critical in maintaining self-tolerance. In this study, we examined the role of PD-1 in a mouse model of acute infection with Histoplasma capsulatum, a major human pathogenic fungus. In a lethal model of histoplasmosis, all PD-1-deficient mice survived infection, whereas the wild-type mice died with disseminated disease. PD-L expression on macrophages and splenocytes was up-regulated during infection, and macrophages from infected mice inhibited in vitro T cell activation. Of interest, antibody blocking of PD-1 significantly increased survival of lethally infected wild-type mice. Thus, our studies extend the role of the PD-1/PD-L pathway in regulating antimicrobial immunity to fungal pathogens. The results show that the PD-1/PD-L pathway has a key role in the regulation of antifungal immunity, and suggest that manipulation of this pathway represents a strategy of immunotherapy for histoplasmosis. | lld:pubmed |
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| pubmed-article:18268348 | pubmed:language | eng | lld:pubmed |
| pubmed-article:18268348 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:18268348 | pubmed:citationSubset | IM | lld:pubmed |
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| pubmed-article:18268348 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:18268348 | pubmed:month | Feb | lld:pubmed |
| pubmed-article:18268348 | pubmed:issn | 1091-6490 | lld:pubmed |
| pubmed-article:18268348 | pubmed:author | pubmed-author:AlmoSteven... | lld:pubmed |
| pubmed-article:18268348 | pubmed:author | pubmed-author:NathensonStan... | lld:pubmed |
| pubmed-article:18268348 | pubmed:author | pubmed-author:FreemanGordon... | lld:pubmed |
| pubmed-article:18268348 | pubmed:author | pubmed-author:GácserAttilaA | lld:pubmed |
| pubmed-article:18268348 | pubmed:author | pubmed-author:NosanchukJosh... | lld:pubmed |
| pubmed-article:18268348 | pubmed:author | pubmed-author:Lázár-MolnárE... | lld:pubmed |
| pubmed-article:18268348 | pubmed:issnType | Electronic | lld:pubmed |
| pubmed-article:18268348 | pubmed:day | 19 | lld:pubmed |
| pubmed-article:18268348 | pubmed:volume | 105 | lld:pubmed |
| pubmed-article:18268348 | pubmed:owner | NLM | lld:pubmed |
| pubmed-article:18268348 | pubmed:authorsComplete | Y | lld:pubmed |
| pubmed-article:18268348 | pubmed:pagination | 2658-63 | lld:pubmed |
| pubmed-article:18268348 | pubmed:dateRevised | 2011-11-17 | lld:pubmed |
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