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Infection and Immunity, November 1998, p. 5457-5461, Vol. 66, No. 11
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.

Gamma Interferon Production by Cytotoxic T Lymphocytes Is Required for Resolution of Chlamydia trachomatis Infection

Mary F. Lampe,1 Christopher B. Wilson,2,3 Michael J. Bevan,3,4 and Michael N. Starnbach5,*

Departments of Laboratory Medicine and Medicine,1 Department of Pediatrics,2 Department of Immunology,3 and Howard Hughes Medical Institute,4 University of Washington, Seattle, Washington 98195, and Department of Microbiology and Molecular Genetics, Harvard Medical School, Boston, Massachusetts 021155

Received 15 May 1998/Returned for modification 23 June 1998/Accepted 7 August 1998

In this study, we used mice in which the gene for gamma interferon (IFN-gamma ) has been disrupted (IFN-gamma -/- mice) to study the role of this cytokine in the resolution of Chlamydia trachomatis infection. We show that IFN-gamma -/- mice are impaired in the ability to clear infection with C. trachomatis compared to IFN-gamma +/+ control mice. Activated CD8+ cytotoxic T lymphocytes (CTL) secrete IFN-gamma in response to intracellular infection, and we have shown previously that a Chlamydia-specific CTL line can reduce C. trachomatis infection when adoptively transferred into infected mice. In the present study, we found that when these IFN-gamma +/+ CTL lines are transferred into Chlamydia-infected IFN-gamma -/- mice, the transferred CTL cannot overcome the immune defect seen in the IFN-gamma -/- mice. We also show that Chlamydia-specific CTL can be cultured from IFN-gamma -deficient mice infected with C. trachomatis; however, the adoptive transfer of IFN-gamma -/- CTL into infected IFN-gamma +/+ mice does not reduce the level of infection. These results suggest that IFN-gamma production by CTL is not sufficient to overcome the defect that IFN-gamma -/- mice have in the resolution of Chlamydia infection, yet IFN-gamma production by CTL is required for the protective effect seen upon adoptive transfer of CTL into IFN-gamma +/+ mice.

* Corresponding author. Mailing address: Department of Microbiology and Molecular Genetics, Harvard Medical School, 200 Longwood Ave., Boston, MA 02115. Phone: (617) 432-1873. Fax: (617) 738-7664. E-mail: starnbach{at}hms.harvard.edu.

Infection and Immunity, November 1998, p. 5457-5461, Vol. 66, No. 11
0019-9567/98/$04.00+0
Copyright © 1998, American Society for Microbiology. All rights reserved.


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