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Journal of Virology, May 2001, p. 4540-4550, Vol. 75, No. 10
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.10.4540-4550.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.

Variation in Adenovirus Transgene Expression between BALB/c and C57BL/6 Mice Is Associated with Differences in Interleukin-12 and Gamma Interferon Production and NK Cell Activation

YuFeng Peng,1 Erik Falck-Pedersen,2 and Keith B. Elkon1,*

Departments of Medicine1 and Microbiology and Immunology,2 Weill Medical College of Cornell University, New York, New York 10021

Received 30 October 2000/Accepted 13 February 2001

The innate immune response against replication-defective adenoviruses (Ad) is poorly defined. We and others have previously observed striking differences in the rate at which the Ad vector itself or the virus encoding a variety of transgenes is eliminated in different mouse strains. Here, we report that Ad infection of BALB/ mice is associated with sixfold-higher levels of serum alanine aminotransferase and that Ad transgenes induce two- to threefold-higher levels of intrahepatic NK cells and NK activity compared to C57BL/6 mice. The increase in NK activation in BALB/c mice was associated with ~4-fold higher level of mRNA expression of a newly described NKG2 receptor activator, H-60, as well as increased expression of interleukin-12 and gamma interferon mRNAs in BALB/c mice compared to C57BL/6 mice. NK depletion in BALB/c mice or defective NK function in C3H beige mice extended transgene expression compared to their appropriate controls, and attenuation of NK together with CD8 T-cell function had a synergistic effect. These findings indicate that there are intrinsic differences in the innate immune responses of different mouse strains to Ad and Ad transgenes and that NK cells, in cooperation with CD8 T cells, play a pivotal role in the early extinction of transgene expression in BALB/c mice.

* Corresponding author. Mailing address: Research Division, Hospital for Special Surgery-Weill Medical College of Cornell University, 535 E. 70th St., New York, NY 10021. Phone: (212) 606-1409. Fax: (212) 774-2337. E-mail: elkonk{at}hss.edu.

Journal of Virology, May 2001, p. 4540-4550, Vol. 75, No. 10
0022-538X/01/$04.00+0   DOI: 10.1128/JVI.75.10.4540-4550.2001
Copyright © 2001, American Society for Microbiology. All rights reserved.


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Copyright © 2001 by the American Society for Microbiology. All rights reserved.