Different roles are played by αβ and γδ T cells in acquired immunity to Chlamydia trachomatis pulmonary infection

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Abstract
Using gene knockout and wild-type C57BL/6 mice, we examined the role of αβ and γδ T cells in the resolution of Chlamydia trachomatis mouse pneumonitis (MoPn) biovar pulmonary infection. The results show that αβ T-cell-deficient (α−/−) mice, when compared with wild-type control mice, have dramatically increased mortality rate and greater in vivo growth of MoPn. The αβ T-cell-deficient mice were as susceptible to MoPn infection as T- and B-lymphocyte-deficient (RAG-1−/−) mice. Moreover, both αβ T-cell-deficient and RAG-1 mutant mice failed to mount delayed-type hypersensitivity (DTH) responses to organism-specific challenge and showed undetectable interferon-γ (IFN-γ) production by spleen cells upon in vitro organism-specific restimulation. In contrast, γδ T-cell-deficient mice exhibited intact DTH responses and their mortality rate and in vivo chlamydial growth were comparable to those in wild-type controls. More interestingly, γδ T-cell-deficient mice showed significantly higher levels of IFN-γ production than did wild-type mice. The data indicate that the αβ T cell is the major T-cell population for acquired immunity to chlamydial infection and that γδ T cells may play an ancillary role in regulating the magnitude of αβ T-cell responses.