The Journal of Experimental Medicine
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Published online 6 August 2001. doi:10.1084/jem.194.3.343
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© The Rockefeller University Press, 0022-1007/2001/8/343/ $5.00
The Journal of Experimental Medicine, Volume 194, Number 3, August 6, 2001 343-354

Original Article

A Critical Role for Interleukin 18 in Primary and Memory Effector Responses to Listeria monocytogenes That Extends Beyond Its Effects on Interferon {gamma} Production

Margaret Neighborsa, Xiuling Xua, Franck J. Barrata, Sigrid R. Ruulsa, Tatyana Churakovab, Reno Debetsb, J. Fernando Bazanb, Robert A. Kasteleinb, John S. Abramsb, and Anne O'Garraa

a Department of Immunology, DNAX Research Institute of Molecular and Cellular Biology, Incorporated, Palo Alto, CA 94304
b Department of Molecular Biology, DNAX Research Institute of Molecular and Cellular Biology, Incorporated, Palo Alto, CA 94304
Dept. of Immunology, DNAX Research Institute, Palo Alto, CA 94304-1104.650-496-1200650-496-1102

margaret.neighbors{at}dnax.org

The stimulation of interferon (IFN)-{gamma} by interleukin (IL)-12 has been shown to provide protection from intracellular pathogens such as Listeria monocytogenes. Tumor necrosis factor (TNF) is also a major player in the resolution of Listeria infections and is suggested to have more global effects than can be explained by the induction of IFN-{gamma} alone. Since IL-18 synergizes with IL-12 to induce IFN-{gamma} production by natural killer and T helper (Th)1 cells, we determined its role in responses to Listeria. IL-18 appeared to be even more potent than either IL-12 or IFN-{gamma} for protection against this pathogen and IL-18 enhanced bacterial clearance in the complete absence of IFN-{gamma}. Indeed IL-18 was comparable to TNF in its ability to resolve the infection and showed a lowered protective capacity in the absence of TNF. Moreover, IL-18 induced macrophages to secrete both TNF and nitric oxide after a Listeria infection. IL-18 was also essential for optimal IFN-{gamma} production by antigen-specific T cells. Therefore, IL-18 operates via its effects on both the innate immune response, including macrophages, as well as on Th1 cells, to protect against Listeria.

Key Words: Listeria • IL-18 • TNF • NO • Th1 cells

Abbreviation used in this paper: HKLM, heat-killed Listeria monocytogenes.

© 2001 The Rockefeller University Press


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