CHLAMYDIA-TRACHOMATIS GENITAL-TRACT INFECTION OF ANTIBODY-DEFICIENT GENE KNOCKOUT MICE

The importance of antibody-mediated immunity in primary and secondary Chlamydia trachomatis genital tract infections was examined by using a definitive model of B-cell deficiency, the mu MT/mu MT gene knockout mouse, Vaginally infected B-cell-deficient mu MT/mu MT mice developed a self-limiting primary infection that was indistinguishable from infe ction of control C57BL/6 mice, Sera and vaginal secretions from infect ed mice were analyzed for anti-Chlamydia antibodies, C57BL/6 mice prod uced high-titered serum anti-Chlamydia immunoglobulin G2a (IgG2a), IgG 2b, and IgA antibodies, and vaginal washes contained predominately ant i-Chlamydia IgA, Serum and vaginal washes from infected B-cell-deficie nt mice were negative for anti-Chlamydia antibody, T-cell proliferatio n and delayed-type hypersensitivity assays were used as measures of Ch lamydia-specific cell-mediated immunity and were found to be comparabl e for C57BL/6 and B-cell-deficient mice, Seventy days following primar y infection, mice were rechallenged to assess acquired immunity, B-cel l-deficient mice which lack anti-Chlamydia antibodies were more suscep tible to reinfection than immunocompetent C57BL/6 mice, However, acqui red immune resistance was evident in both strains of mice and characte rized by decreased shedding of chlamydiae and an infection of shorter duration, Thus, this study demonstrates that cell-mediated immune resp onses alone were capable of resolving chlamydial infection; however, i n the absence of specific antibody, mice were more susceptible to rein fection, Therefore, these data suggest that both humoral and cell-medi ated immune responses were important mediators of immune protection in this model, though cell-mediated immune responses appear to play a mo re dominant role.