| pubmed-article:19380790 | rdf:type | pubmed:Citation | lld:pubmed |
| pubmed-article:19380790 | lifeskim:mentions | umls-concept:C0007684 | lld:lifeskim |
| pubmed-article:19380790 | lifeskim:mentions | umls-concept:C0026538 | lld:lifeskim |
| pubmed-article:19380790 | lifeskim:mentions | umls-concept:C0449297 | lld:lifeskim |
| pubmed-article:19380790 | lifeskim:mentions | umls-concept:C0851285 | lld:lifeskim |
| pubmed-article:19380790 | lifeskim:mentions | umls-concept:C1880177 | lld:lifeskim |
| pubmed-article:19380790 | pubmed:issue | 9 | lld:pubmed |
| pubmed-article:19380790 | pubmed:dateCreated | 2009-4-21 | lld:pubmed |
| pubmed-article:19380790 | pubmed:abstractText | The neurotropic coronavirus JHM strain of mouse hepatitis virus persists in oligodendroglia despite the presence of virus-specific CD8 T cells. Expression of programmed death 1 (PD-1) and B7-H1 were studied during acute and persistent infection to examine whether this negative regulatory mechanism contributes to CNS viral persistence. The majority of CNS-infiltrating CD8 T cells expressed PD-1, with the highest levels on virus-specific CD8 T cells. Moreover, despite control of infectious virus, CD8 T cells within the CNS of persistently infected mice maintained high PD-1 expression. Analysis of virus-susceptible target cells in vivo revealed that B7-H1 expression was regulated in a cell type-dependent manner. Oligodendroglia and microglia up-regulated B7-H1 following infection; however, although B7-H1 expression on oligodendroglia was prominent and sustained, it was significantly reduced and transient on microglia. Infection of mice deficient in the IFN-gamma or IFN-alpha/beta receptor demonstrated that B7-H1 expression on oligodendroglia is predominantly regulated by IFN-gamma. Ab blockade of B7-H1 on oligodendroglia in vitro enhanced IFN-gamma secretion by virus-specific CD8 T cells. More efficient virus control within the CNS of B7-H1-deficient mice confirmed inhibition of CD8 T cell function in vivo. Nevertheless, the absence of B7-H1 significantly increased morbidity without altering demyelination. These data are the first to demonstrate glia cell type-dependent B7-H1 regulation in vivo, resulting in adverse effects on antiviral CD8 T cell function. However, the beneficial role of PD-1:B7-H1 interactions in limiting morbidity highlights the need to evaluate tissue-specific intervention strategies. | lld:pubmed |
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| pubmed-article:19380790 | pubmed:language | eng | lld:pubmed |
| pubmed-article:19380790 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
| pubmed-article:19380790 | pubmed:citationSubset | AIM | lld:pubmed |
| pubmed-article:19380790 | pubmed:chemical | http://linkedlifedata.com/r... | lld:pubmed |
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| pubmed-article:19380790 | pubmed:status | MEDLINE | lld:pubmed |
| pubmed-article:19380790 | pubmed:month | May | lld:pubmed |
| pubmed-article:19380790 | pubmed:issn | 1550-6606 | lld:pubmed |
| pubmed-article:19380790 | pubmed:author | pubmed-author:ChenLiepingL | lld:pubmed |
| pubmed-article:19380790 | pubmed:author | pubmed-author:RamakrishnaCh... | lld:pubmed |
| pubmed-article:19380790 | pubmed:author | pubmed-author:StohlmanSteph... | lld:pubmed |
| pubmed-article:19380790 | pubmed:author | pubmed-author:BergmannCorne... | lld:pubmed |
| pubmed-article:19380790 | pubmed:author | pubmed-author:AtkinsonRosco... | lld:pubmed |
| pubmed-article:19380790 | pubmed:author | pubmed-author:PharesTimothy... | lld:pubmed |
| pubmed-article:19380790 | pubmed:author | pubmed-author:ParraGabriel... | lld:pubmed |
| pubmed-article:19380790 | pubmed:author | pubmed-author:EpsteinAlanA | lld:pubmed |
| pubmed-article:19380790 | pubmed:issnType | Electronic | lld:pubmed |
