|
|
||||||||
Published online before print June 10, 2005
| ||||||||||||||||||||||||||||||||||||||||||||||||||||||||||||
Article |
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
| HOME | HELP | FEEDBACK | SUBSCRIPTIONS | ARCHIVE | SEARCH |