DIFFERENT ROLES ARE PLAYED BY ALPHA-BETA AND GAMMA-DELTA T-CELLS IN ACQUIRED-IMMUNITY TO CHLAMYDIA-TRACHOMATIS PULMONARY INFECTION

Using gene knockout and wild-type C57BL/6 mice, we examined the role o f alpha beta and gamma delta T cells in the resolution of Chlamydia tr achomatis mouse pneumonitis (MoPn) biovar pulmonary infection. The res ults show that alpha beta T-cell-deficient (alpha(-/-)) mice, when com pared with wild-type control mice, have dramatically increased mortali ty rate and greater in vivo growth of MoPn. The alpha beta T-cell-defi cient mice were as susceptible to MoPn infection as T- and B-lymphocyt e-deficient (RAG-1(-/-)) mice. Moreover. both alpha beta T-cell-defici ent and RAG-1 mutant mice failed to mount delayed-type hypersensitivit y (DTH) responses to organism-specific challenge and showed undetectab le interferon-gamma (IFN-gamma) production by spleen cells upon in vit ro organism-specific restimulation. In contrast, gamma delta T-cell-de ficient mice exhibited intact DTH responses and their mortality rate a nd in vivo chlamydial growth were comparable to those in wild-type con trols. More interestingly, gamma delta T-cell-deficient mice showed si gnificantly higher levels of IFN-gamma production than did wild-type m ice. The data indicate that the alpha beta T cell is the major T-cell population for acquired immunity to chlamydial infection and that gamm a delta T cells may play an ancillary role in regulating the magnitude of alpha beta T-cell responses.