Abstract |
We had previously reported that freshly harvested peritoneal macrophages (PM) are in a type I IFN-mediated antiviral state, which is lost during in vitro culture of PM, concomitantly with a progressive decline in the expression of IFN-beta. We report herein that in vitro culture of PM in the presence of IL-4 or IL-10 results in an enhanced decay of the IFN-beta-mediated antiviral state to vesicular stomatitis virus (VSV). Moreover, IL-4 and IL-10 inhibited the production of type I IFN induced by LPS or NDV infection, as assessed by IFN production and induction of IFN-mediated antiviral state. The accumulation and physiological turnover of IFN-beta mRNA was not affected by IL-4 or IL-10. Finally, neither IL-10 nor IL-4 exerted any inhibitory effect on the antiviral activity induced by exogenous type-I IFN. These results suggest that Th2 cytokines, such as IL-4 and IL-10, act as negative regulators of the type I IFN-mediated antiviral response in PM and may represent stop signals for the constitutive or induced type I IFN expression in PM.
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Authors | B Varano, L Fantuzzi, P Puddu, P Borghi, F Belardelli, S Gessani |
Journal | Virology
(Virology)
Vol. 277
Issue 2
Pg. 270-7
(Nov 25 2000)
ISSN: 0042-6822 [Print] United States |
PMID | 11080475
(Publication Type: Journal Article)
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Copyright | Copyright 2000 Academic Press. |
Chemical References |
- Lipopolysaccharides
- RNA, Messenger
- Interleukin-10
- Interleukin-4
- Interferon-beta
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Topics |
- Animals
- Cells, Cultured
- Dose-Response Relationship, Drug
- Down-Regulation
- Interferon-beta
(biosynthesis, genetics)
- Interleukin-10
(pharmacology)
- Interleukin-4
(pharmacology)
- Lipopolysaccharides
- Macrophages, Peritoneal
(drug effects, immunology, virology)
- Male
- Mice
- Mice, Inbred C3H
- Newcastle disease virus
- RNA, Messenger
(genetics)
- Specific Pathogen-Free Organisms
- Time Factors
- Vesicular stomatitis Indiana virus
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