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Inhibition of the constitutive and induced IFN-beta production by IL-4 and IL-10 in murine peritoneal macrophages
B Varano1, L Fantuzzi, P Puddu
1Laboratory of Virology, Istituto Superiore di Sanità, Viale Regina Elena 299, 00161 Rome, Italy.
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.
Insights
Interleukin-4 (IL-4) and Interleukin-10 (IL-10) cytokines suppress the type I interferon (IFN)-mediated antiviral state in peritoneal macrophages (PM). These Th2 cytokines act as negative regulators, potentially halting IFN expression in macrophages.
Area of Science:
- Immunology
- Cell Biology
- Virology
Background:
- Freshly harvested peritoneal macrophages (PM) exhibit a type I interferon (IFN)-mediated antiviral state.
- This antiviral state is diminished during in vitro culture, correlating with reduced IFN-beta expression.
Purpose of the Study:
- To investigate the effect of IL-4 and IL-10 on the IFN-beta-mediated antiviral state in PM.
- To determine if IL-4 and IL-10 modulate type I IFN production or response in PM.
Main Methods:
- In vitro culture of PM with IL-4 or IL-10.
- Assessment of antiviral state decay against vesicular stomatitis virus (VSV).
- Measurement of type I IFN production induced by lipopolysaccharide (LPS) or Newcastle disease virus (NDV).
- Analysis of IFN-beta mRNA levels and response to exogenous type I IFN.
Main Results:
- IL-4 and IL-10 accelerated the decay of the IFN-beta-mediated antiviral state in PM.
- These cytokines inhibited type I IFN production induced by LPS or NDV.
- IL-4 and IL-10 did not affect IFN-beta mRNA turnover or the antiviral activity of exogenous type I IFN.
Conclusions:
- Th2 cytokines, IL-4 and IL-10, act as negative regulators of the type I IFN-mediated antiviral response in PM.
- These cytokines may function as 'stop signals' for constitutive or induced type I IFN expression in macrophages.
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