pubmed-article:20123961 | rdf:type | pubmed:Citation | lld:pubmed |
pubmed-article:20123961 | lifeskim:mentions | umls-concept:C0023861 | lld:lifeskim |
pubmed-article:20123961 | lifeskim:mentions | umls-concept:C0024426 | lld:lifeskim |
pubmed-article:20123961 | lifeskim:mentions | umls-concept:C0205263 | lld:lifeskim |
pubmed-article:20123961 | pubmed:issue | 2 | lld:pubmed |
pubmed-article:20123961 | pubmed:dateCreated | 2010-2-16 | lld:pubmed |
pubmed-article:20123961 | pubmed:abstractText | Production of type I interferon (IFN; IFN-alphabeta) increases host susceptibility to Listeria monocytogenes, whereas type II IFN (IFN-gamma) activates macrophages to resist infection. We show that these opposing immunological effects of IFN-alphabeta and IFN-gamma occur because of cross talk between the respective signaling pathways. We found that cultured macrophages infected with L. monocytogenes were refractory to IFN-gamma treatment as a result of down-regulation of the IFN-gamma receptor (IFNGR). The soluble factor responsible for these effects was identified as host IFN-alphabeta. Accordingly, macrophages and dendritic cells (DCs) showed reduced IFNGR1 expression and reduced responsiveness to IFN-gamma during systemic infection of IFN-alphabeta-responsive mice. Furthermore, the increased resistance of mice lacking the IFN-alphabeta receptor (IFNAR(-/-)) to L. monocytogenes correlated with increased expression of IFN-gamma-dependent activation markers by macrophages and DCs and was reversed by depletion of IFN-gamma. Thus, IFN-alphabeta produced in response to bacterial infection and other stimuli antagonizes the host response to IFN-gamma by down-regulating the IFNGR. Such cross talk permits prioritization of IFN-alphabeta-type immune responses and may contribute to the beneficial effects of IFN-beta in treatment of inflammatory diseases such as multiple sclerosis. | lld:pubmed |
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pubmed-article:20123961 | pubmed:language | eng | lld:pubmed |
pubmed-article:20123961 | pubmed:journal | http://linkedlifedata.com/r... | lld:pubmed |
pubmed-article:20123961 | pubmed:citationSubset | IM | lld:pubmed |
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pubmed-article:20123961 | pubmed:status | MEDLINE | lld:pubmed |
pubmed-article:20123961 | pubmed:month | Feb | lld:pubmed |
pubmed-article:20123961 | pubmed:issn | 1540-9538 | lld:pubmed |
pubmed-article:20123961 | pubmed:author | pubmed-author:PenheiterKris... | lld:pubmed |
pubmed-article:20123961 | pubmed:author | pubmed-author:LenzLaurel... | lld:pubmed |
pubmed-article:20123961 | pubmed:author | pubmed-author:HumannJessica... | lld:pubmed |
pubmed-article:20123961 | pubmed:author | pubmed-author:AndreasenKarl... | lld:pubmed |
pubmed-article:20123961 | pubmed:author | pubmed-author:RayamajhiMani... | lld:pubmed |
pubmed-article:20123961 | pubmed:issnType | Electronic | lld:pubmed |
pubmed-article:20123961 | pubmed:day | 15 | lld:pubmed |
pubmed-article:20123961 | pubmed:volume | 207 | lld:pubmed |
pubmed-article:20123961 | pubmed:owner | NLM | lld:pubmed |
pubmed-article:20123961 | pubmed:authorsComplete | Y | lld:pubmed |
pubmed-article:20123961 | pubmed:pagination | 327-37 | lld:pubmed |
pubmed-article:20123961 | pubmed:dateRevised | 2011-5-5 | lld:pubmed |
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pubmed-article:20123961 | pubmed:year | 2010 | lld:pubmed |
pubmed-article:20123961 | pubmed:articleTitle | Induction of IFN-alphabeta enables Listeria monocytogenes to suppress macrophage activation by IFN-gamma. | lld:pubmed |
pubmed-article:20123961 | pubmed:affiliation | National Jewish Health, Denver, CO 80206, USA. | lld:pubmed |
pubmed-article:20123961 | pubmed:publicationType | Journal Article | lld:pubmed |
pubmed-article:20123961 | pubmed:publicationType | Research Support, N.I.H., Extramural | lld:pubmed |
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