Source:http://linkedlifedata.com/resource/pubmed/id/18566423
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| Predicate | Object |
|---|---|
| rdf:type | |
| lifeskim:mentions |
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umls-concept:C1706817,
umls-concept:C1710082,
umls-concept:C2911692
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| pubmed:issue |
1
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| pubmed:dateCreated |
2008-6-20
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| pubmed:abstractText |
The antiviral activities of type I IFNs have long been established. However, comparatively little is known of their role in defenses against nonviral pathogens. We examined here the effects of type I IFNs on host resistance against the model pathogenic yeast Cryptococcus neoformans. After intratracheal or i.v. challenge with this fungus, most mice lacking either the IFN-alpha/beta receptor (IFN-alpha/betaR) or IFN-beta died from unrestrained pneumonia and encephalitis, while all wild-type controls survived. The pulmonary immune response of IFN-alpha/betaR-/- mice was characterized by increased expression of IL-4, IL-13, and IL-10, decreased expression of TNF-alpha, IFN-gamma, inducible NO synthetase, and CXCL10, and similar levels of IL-12 mRNA, compared with wild-type controls. Histopathological analysis showed eosinophilic infiltrates in the lungs of IFN-alpha/betaR-/- mice, although this change was less extensive than that observed in similarly infected IFN-gammaR-deficient animals. Type I IFN responses could not be detected in the lung after intratracheal challenge. However, small, but statistically significant, elevations in IFN-beta levels were measured in the supernatants of bone marrow-derived macrophages or dendritic cells infected with C. neoformans. Our data demonstrate that type I IFN signaling is required for polarization of cytokine responses toward a protective type I pattern during cryptococcal infection.
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| pubmed:language |
eng
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| pubmed:journal | |
| pubmed:citationSubset |
AIM
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| pubmed:chemical | |
| pubmed:status |
MEDLINE
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| pubmed:month |
Jul
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| pubmed:issn |
0022-1767
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| pubmed:author |
pubmed-author:BellantoniAntonellaA,
pubmed-author:BeninatiConcettaC,
pubmed-author:BiondoCarmeloC,
pubmed-author:FaldutoMariaM,
pubmed-author:GalboRobertaR,
pubmed-author:GambuzzaMariaM,
pubmed-author:GeraceElisabettaE,
pubmed-author:LeandersonTomasT,
pubmed-author:MancusoGiuseppeG,
pubmed-author:MidiriAngelinaA,
pubmed-author:TetiGiuseppeG
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| pubmed:issnType |
Print
|
| pubmed:day |
1
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| pubmed:volume |
181
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| pubmed:owner |
NLM
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| pubmed:authorsComplete |
Y
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| pubmed:pagination |
566-73
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| pubmed:meshHeading |
pubmed-meshheading:18566423-Animals,
pubmed-meshheading:18566423-Cells, Cultured,
pubmed-meshheading:18566423-Cryptococcosis,
pubmed-meshheading:18566423-Dendritic Cells,
pubmed-meshheading:18566423-Disease Models, Animal,
pubmed-meshheading:18566423-Interferon-alpha,
pubmed-meshheading:18566423-Interferon-beta,
pubmed-meshheading:18566423-Macrophages,
pubmed-meshheading:18566423-Mice,
pubmed-meshheading:18566423-Mice, Inbred C57BL,
pubmed-meshheading:18566423-Mice, Knockout,
pubmed-meshheading:18566423-Receptor, Interferon alpha-beta,
pubmed-meshheading:18566423-Signal Transduction,
pubmed-meshheading:18566423-Survival Rate
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| pubmed:year |
2008
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| pubmed:articleTitle |
IFN-alpha/beta signaling is required for polarization of cytokine responses toward a protective type 1 pattern during experimental cryptococcosis.
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| pubmed:affiliation |
Dipartimento di Patologia e Microbiologia Sperimentale, Università degli Studi di Messina, Messina, Italy.
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| pubmed:publicationType |
Journal Article
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