B-cell-deficient mice develop complete immune protection against genital tract infection with <em> Chlamydia trachomatis </em>.

We evaluated the ability of mice made genetically deficient for B cells to resolve a primary infection and to develop protective immunity against vaginal challenge with a human isolate of Chlamydia trachomatis bacteria. The B-cell-deficient μMT mice cleared a primary ascending infection with similar or faster kinetics compared with wild-type mice. The presence of chlamydial inclusion bodies and the degree of inflammation in the upper genital tract was comparable and showed similar kinetics in μMT as in wild-type mice. Following resolution of the primary infection the mice were challenged by 100 ID₅₀ of live bacteria and the level of protection and the extent of local inflammation was assessed. Strikingly, all μMT mice, as well as most of the wild-type mice, demonstrated complete immune protection with no bacterial shedding. While high titres of chlamydia-specific antibodies were stimulated locally and systemically in wild-type mice, no antibodies were detected in μMT mice. However, in both strains, immunohistochemical analysis of the upper genital tract demonstrated the presence of large numbers of CD4⁺ T cells and increased levels of interferon-γ (IFN-γ)-producing cells. The results unequivocally demonstrate that antibodies are not required for full protection to develop against ascending infection with a high dose of C. trachomatis in the female genital tract. Our study confirms the notion that cell-mediated immunity, in particular that owing to CD4⁺ T helper 1 (Th1)-type cells, is critical for host resistance against C. trachoinatis in mice. [ABSTRACT FROM AUTHOR]