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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,
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-
)
production (days 3 and 5) but not late T-cell-dependent IFN-
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.

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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