Published online before print June 10, 2005

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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.0105035

Received for publication January 21, 2005.
Revised April 29, 2005.
Accepted for publication May 12, 2005.

Article

IL-2 induces expression and secretion of IFN- in murine peritoneal macrophages

Department of Cell Biology and Neurosciences, Istituto Superiore di Sanità, Rome, Italy

^@ To whom correspondence should be addressed. E-mail: gessani{at}iss.it.

Abstract

We investigated the effect of interleukin (IL)-2, a T cell growth factor capable of activating certain macrophage functions, on interferon (IFN)- expression in resting mouse peritoneal macrophages (PM). IL-2 addition to PM from different mouse strains up-modulated IFN- mRNA and protein secretion. It is notable that endogenous type I and II IFNs did not play any role in the IL-2-mediated effect, as comparable levels of secreted IFN- were observed upon IL-2 stimulation of PM from deficient mice. In contrast, endogenous IFN- was requested for the IL-12-induced IFN- production. It is interesting that blocking of each component of the IL-2 receptor (IL-2R) by neutralizing antibodies almost completely abolished IL-2-induced IFN- production, suggesting that all IL-2R chains contribute to the PM biological response to IL-2. The simultaneous treatment of PM with IL-2 and IL-12 resulted in a higher IFN- secretion with respect to that obtained upon treatment with IL-2 or IL-12 alone. It is notable that IFN- protein was expressed intracellularly in the majority of cells exhibiting a macrophage phenotype (i.e., F4/80⁺) and was secreted upon IL-2 stimulation. Overall, these findings demonstrate that IL-2 regulates at different levels IFN- expression in macrophages, highlighting the crucial role of these cells and their regulated responsiveness to key cytokines in the cross-talk between innate and adaptive immunity.

Key Words: cytokine secretion • mouse • gene regulation

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