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

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.