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J Virol, June 1998, p. 4825-4831, Vol. 72, No. 6
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Role of Interleukin-12 in Primary Influenza Virus Infection

Juanita M. Monteiro,1,dagger Catherine Harvey,2 and Giorgio Trinchieri1,*

Wistar Institute of Anatomy and Biology, Philadelphia, Pennsylvania 19104,1 and University of Wisconsin, Madison, Wisconsin 535902

Received 15 September 1997/Accepted 10 March 1998

The effect of endogenous interleukin-12 (IL-12) on the influenza virus immune response in BALB/c mice was evaluated. Following primary influenza virus infection, IL-12 mRNA and protein are detected in the lung, with live virus being required for cytokine induction. Endogenous IL-12 contributes to early NK cell-dependent gamma interferon (IFN-gamma ) production (days 3 and 5) but not late T-cell-dependent IFN-gamma secretion (day 7). IL-12 contributes to the inhibition of early virus replication but is not required for virus clearance. IL-12 also modestly contributes to the activation of cytotoxic T lymphocytes. Thus, in this model of experimental influenza virus infection, endogenous IL-12 contributes primarily to the early development and activation of the innate immune response.

* Corresponding author. Mailing address: The Wistar Institute, 3601 Spruce St., Philadelphia, PA 19104. Phone: (215) 898-3992. Fax: (215) 898-2357. E-mail: trinchieri{at}wista.wistar.upenn.edu.

dagger Present address: Merck Research Laboratories, Merck & Co., Inc., West Point, Pa.

J Virol, June 1998, p. 4825-4831, Vol. 72, No. 6
0022-538X/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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