| http://purl.uniprot.org/citations/19124736 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/19124736 | http://www.w3.org/2000/01/rdf-schema#comment | "A critical issue during severe respiratory infection is whether it is the virus or the host response that does the most damage. In this study, we show that endogenous 4-1BBL plays a critical role in protecting mice from severe effects of influenza disease. During mild respiratory influenza infection in which virus is rapidly cleared, the inducible costimulatory receptor 4-1BB is only transiently induced on lung T cells and 4-1BB ligand (4-1BBL) is completely dispensable for the initial CD8 T cell response and mouse survival. In contrast, during more severe respiratory influenza infection with prolonged viral load, 4-1BB expression on lung CD8 T cells is sustained, and 4-1BBL-deficient mice show decreased CD8 T cell accumulation in the lungs, decreased viral clearance, impaired lung function, and increased mortality. Transfer of an optimal number of naive Ag-specific T cells before infection protects wild-type but not 4-1BBL-deficient mice from an otherwise lethal dose of influenza virus. Transfer of T cells lacking the proapoptotic molecule Bim extends the lifespan of 4-1BBL-deficient mice by one to three days, suggesting that at least part of the role of 4-1BB/4-1BBL is to prolong effector cell survival long enough to clear virus. Intranasal delivery of 4-1BBL by recombinant adenovirus marginally improves survival of 4-1BBL-deficient mice at low dose, but exacerbates disease at high dose. These findings suggest a rationale for the evolutionary accumulation of inducible costimulatory molecules, thereby allowing the immune system to sustain the expression of molecules such as 4-1BB to a level commensurate with severity of infection."xsd:string |
| http://purl.uniprot.org/citations/19124736 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.182.2.934"xsd:string |
| http://purl.uniprot.org/citations/19124736 | http://purl.uniprot.org/core/author | "Moraes T.J."xsd:string |
| http://purl.uniprot.org/citations/19124736 | http://purl.uniprot.org/core/author | "Watts T.H."xsd:string |
| http://purl.uniprot.org/citations/19124736 | http://purl.uniprot.org/core/author | "Sedgmen B.J."xsd:string |
| http://purl.uniprot.org/citations/19124736 | http://purl.uniprot.org/core/author | "Lin G.H."xsd:string |
| http://purl.uniprot.org/citations/19124736 | http://purl.uniprot.org/core/author | "Topham D.J."xsd:string |
| http://purl.uniprot.org/citations/19124736 | http://purl.uniprot.org/core/author | "Snell L.M."xsd:string |
| http://purl.uniprot.org/citations/19124736 | http://purl.uniprot.org/core/date | "2009"xsd:gYear |
| http://purl.uniprot.org/citations/19124736 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/19124736 | http://purl.uniprot.org/core/pages | "934-947"xsd:string |
| http://purl.uniprot.org/citations/19124736 | http://purl.uniprot.org/core/title | "Endogenous 4-1BB ligand plays a critical role in protection from influenza-induced disease."xsd:string |
| http://purl.uniprot.org/citations/19124736 | http://purl.uniprot.org/core/volume | "182"xsd:string |
| http://purl.uniprot.org/citations/19124736 | http://www.w3.org/2004/02/skos/core#exactMatch | http://purl.uniprot.org/pubmed/19124736 |
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