HOME HELP FEEDBACK SUBSCRIPTIONS ARCHIVE SEARCH		QUICK SEARCH:   [advanced] Author: Keyword(s): Year:  Vol:  Page:

Published online before print June 10, 2005

This Article Full Text (Reprint (PDF)) All Versions of this Article: jlb.0105035v1 78/3/686    most recent Alert me when this article is cited Alert me if a correction is posted Services Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via Google Scholar Google Scholar Articles by Puddu, P. Articles by Gessani, S. Search for Related Content PubMed PubMed Citation Articles by Puddu, P. Articles by Gessani, S.

© 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

This article has been cited by other articles:

				Z. Li, F. Pradera, T. Kammertoens, B. Li, S. Liu, and Z. Qin Cross-Talk between T Cells and Innate Immune Cells Is Crucial for IFN-{gamma}-Dependent Tumor Rejection J. Immunol., August 1, 2007; 179(3): 1568 - 1576. [Abstract] [Full Text] [PDF]

				L. Li, L. Huang, S.-s. J. Sung, P. I. Lobo, M. G. Brown, R. K. Gregg, V. H. Engelhard, and M. D. Okusa NKT Cell Activation Mediates Neutrophil IFN-{gamma} Production and Renal Ischemia-Reperfusion Injury J. Immunol., May 1, 2007; 178(9): 5899 - 5911. [Abstract] [Full Text] [PDF]

				J. T. Murphy, S. Sommer, E. A. Kabara, N. Verman, M. A. Kuelbs, P. Saama, R. Halgren, and P. M. Coussens Gene expression profiling of monocyte-derived macrophages following infection with Mycobacterium avium subspecies avium and Mycobacterium avium subspecies paratuberculosis Physiol Genomics, December 13, 2006; 28(1): 67 - 75. [Abstract] [Full Text] [PDF]