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rdf:type |
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lifeskim:mentions |
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pubmed:issue |
2
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pubmed:dateCreated |
2010-2-16
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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.
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pubmed:grant |
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pubmed:commentsCorrections |
http://linkedlifedata.com/resource/pubmed/commentcorrection/20123961-10030838,
http://linkedlifedata.com/resource/pubmed/commentcorrection/20123961-10202937,
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http://linkedlifedata.com/resource/pubmed/commentcorrection/20123961-9058823
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pubmed:language |
eng
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pubmed:journal |
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pubmed:citationSubset |
IM
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pubmed:chemical |
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pubmed:status |
MEDLINE
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pubmed:month |
Feb
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pubmed:issn |
1540-9538
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pubmed:author |
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pubmed:issnType |
Electronic
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pubmed:day |
15
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pubmed:volume |
207
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
327-37
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pubmed:dateRevised |
2011-5-5
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pubmed:meshHeading |
pubmed-meshheading:20123961-Animals,
pubmed-meshheading:20123961-Cells, Cultured,
pubmed-meshheading:20123961-Dendritic Cells,
pubmed-meshheading:20123961-Down-Regulation,
pubmed-meshheading:20123961-Female,
pubmed-meshheading:20123961-Immunity, Innate,
pubmed-meshheading:20123961-Interferon Type I,
pubmed-meshheading:20123961-Interferon-gamma,
pubmed-meshheading:20123961-Listeria monocytogenes,
pubmed-meshheading:20123961-Listeriosis,
pubmed-meshheading:20123961-Macrophage Activation,
pubmed-meshheading:20123961-Macrophages,
pubmed-meshheading:20123961-Mice,
pubmed-meshheading:20123961-Receptors, Interferon
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pubmed:year |
2010
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pubmed:articleTitle |
Induction of IFN-alphabeta enables Listeria monocytogenes to suppress macrophage activation by IFN-gamma.
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pubmed:affiliation |
National Jewish Health, Denver, CO 80206, USA.
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pubmed:publicationType |
Journal Article,
Research Support, N.I.H., Extramural
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