Immunity, immunopathology, and human vaccine development against sexually transmitted Chlamydia trachomatis

This review examines the immunity, immunopathology, and contemporary problems of vaccine development against sexually transmitted Chlamydia trachomatis. Despite improved surveillance and treatment initiatives, the incidence of C. trachomatis infection has increased dramatically over the past 30 years in both the developed and developing world. Studies in animal models have shown that protective immunity to C. trachomatis is largely mediated by Th1 T cells producing IFN-γ which is needed to prevent dissemination of infection. Similar protection appears to develop in humans but in contrast to mice, immunity in humans may take years to develop. Animal studies and evidence from human infection indicate that immunity to C. trachomatis is accompanied by significant pathology in the upper genital tract. Although no credible evidence is currently available to indicate that autoimmunity plays a role, nevertheless, this underscores the necessity to design vaccines strictly based on chlamydial-specific antigens and to avoid those displaying even minimal sequence homologies with host molecules. Current advances in C. trachomatis vaccine development as well as alternatives for designing new vaccines for this disease are discussed. A novel approach for chlamydia vaccine development, based on targeting endogenous dendritic cells, is described.