Gamma interferon production by cytotoxic T lymphocytes is required for resolution of Chlamydia trachomatis infection

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.