The Journal of Experimental Medicine
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Published 2 August 2004. doi:10.1084/jem.20040370
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 200, Number 3, 287-295
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A Contribution of Mouse Dendritic Cell–Derived IL-2 for NK Cell Activation

Francesca Granucci1, Ivan Zanoni1, Norman Pavelka1, Serani L.H. van Dommelen2, Christopher E. Andoniou2, Filippo Belardelli3, Mariapia A. Degli Esposti2, and Paola Ricciardi-Castagnoli1

1 Department of Biotechnology and Bioscience, University of Milano-Bicocca, 20126 Milan, Italy
2 Immunology and Virology Program, Centre for Ophthalmology and Visual Sciences, The University of Western Australia and Centre for Experimental Immunology, Lions Eye Institute, Perth 6009, Western Australia, Australia
3 Laboratory of Virology, Istituto Superiore di Sanità, 00100 Rome, Italy

Address correspondence to Paola Ricciardi-Castagnoli, Dept. of Biotechnology and Bioscience, University of Milano–Bicocca Piazza della Scienza, 2, 20126 Milano, Italy. Phone: 39-02-64483559; Fax: 39-02-64483552; email: paola.castagnoli{at}unimib.it

Dendritic cells (DCs) play a predominant role in activation of natural killer (NK) cells that exert their functions against pathogen-infected and tumor cells. Here, we used a murine model to investigate the molecular mechanisms responsible for this process. Two soluble molecules produced by bacterially activated myeloid DCs are required for optimal priming of NK cells. Type I interferons (IFNs) promote the cytotoxic functions of NK cells. IL-2 is necessary both in vitro and in vivo for the efficient production of IFN{gamma}, which has an important antimetastatic and antibacterial function. These findings provide new information about the mechanisms that mediate DC–NK cell interactions and define a novel and fundamental role for IL-2 in innate immunity.

Key Words: NK cells • dendritic cells • innate immune response • interleukin 2 • interferon {gamma}

F. Granucci and I. Zanoni contributed equally to this work.


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