| http://purl.uniprot.org/citations/21940678 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/21940678 | http://www.w3.org/2000/01/rdf-schema#comment | "An immune response of appropriate magnitude should be robust enough to control pathogen spread but not simultaneously lead to immunopathology. Primary infection with influenza A virus (IAV) results in a localized pulmonary infection and inflammation and elicits an IAV-specific CD8 T cell immune response necessary for viral clearance. Clearance of IAV-infected cells, and recovery from infection, is mediated by perforin/granzyme B- and Fas/FasL-mediated mechanisms. We recently reported that TRAIL is another means by which IAV-specific CD8 T cells can kill IAV-infected cells. The current study examined the role of TRAIL in the pulmonary CD8 T cell response to a clinically significant IAV [A/PR/8/34 (PR8; H1N1)] infection (i.e., leads to observable, but limited, morbidity and mortality in wild-type [WT] mice). Compared with WT mice, IAV-infected Trail(-/-) mice experienced increased morbidity and mortality despite similar rates of viral clearance from the lungs. The increased morbidity and mortality in Trail(-/-) mice correlated with increased pulmonary pathology and inflammatory chemokine production. Analysis of lung-infiltrating lymphocytes revealed increased numbers of IAV-specific CD8 T cells in infected Trail(-/-) mice, which correlated with increased pulmonary cytotoxic activity and increased pulmonary expression of MIG and MIP-1α. In addition, there was decreased apoptosis and increased proliferation of IAV-specific CD8 T cells in the lungs of Trail(-/-) mice compared with WT mice. Together, these data suggest that TRAIL regulates the magnitude of the IAV-specific CD8 T cell response during a clinically significant IAV infection to decrease the chance for infection-induced immunopathology."xsd:string |
| http://purl.uniprot.org/citations/21940678 | http://purl.org/dc/terms/identifier | "doi:10.4049/jimmunol.1002241"xsd:string |
| http://purl.uniprot.org/citations/21940678 | http://purl.uniprot.org/core/author | "Gurung P."xsd:string |
| http://purl.uniprot.org/citations/21940678 | http://purl.uniprot.org/core/author | "Griffith T.S."xsd:string |
| http://purl.uniprot.org/citations/21940678 | http://purl.uniprot.org/core/author | "Legge K.L."xsd:string |
| http://purl.uniprot.org/citations/21940678 | http://purl.uniprot.org/core/author | "Brincks E.L."xsd:string |
| http://purl.uniprot.org/citations/21940678 | http://purl.uniprot.org/core/author | "Langlois R.A."xsd:string |
| http://purl.uniprot.org/citations/21940678 | http://purl.uniprot.org/core/author | "Hemann E.A."xsd:string |
| http://purl.uniprot.org/citations/21940678 | http://purl.uniprot.org/core/date | "2011"xsd:gYear |
| http://purl.uniprot.org/citations/21940678 | http://purl.uniprot.org/core/name | "J Immunol"xsd:string |
| http://purl.uniprot.org/citations/21940678 | http://purl.uniprot.org/core/pages | "4581-4588"xsd:string |
| http://purl.uniprot.org/citations/21940678 | http://purl.uniprot.org/core/title | "The magnitude of the T cell response to a clinically significant dose of influenza virus is regulated by TRAIL."xsd:string |
| http://purl.uniprot.org/citations/21940678 | http://purl.uniprot.org/core/volume | "187"xsd:string |
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