Immunity against chlamydia trachomatis

Abstract

Chlamydia trachomatis, the etiology of one of the most common human infections, is responsible for an increasing number of genital tract infections world-wide. In addition, this obligate intracellular pathogen infects epithelial cells of the eye, resulting in trachoma and, as a sequela, blindness. The genital tract infection often leads to severe damage of the reproductive tract, resulting in tubal factor infertility. Infection of the genital tract stimulates a complex array of host immune responses involving innate as well as adaptive immune responses. Cells of the innate immune system recognize and limit the spread of infection, and influence the outcome of infection through the modulation of the adaptive immune response. Protective immunity against C. trachomatis involves primarily Th1 CD4+ T cells and IFN-γ production, while antibodies, and possibly CD8+ T cells, can contribute to protection. However, the immune response to infection is complex and those components that convey protective immunity may contribute to the pathogenesis. Therefore, it is believed that a balance between Th1/Th2 effector and regulatory T cell populations is required to avoid harmful immunopathology and permanent sequelae. Advances in our understanding of the immunobiology of the genital tract and better knowledge about chlamydial infections are key issues for the development of effective vaccines. In this context, identifying protective chlamydial antigens is crucial as well as investigating optimal immunization routes and vaccine formulations, including choice of adjuvant, will probably be central to an effective anti-chlamydial vaccine. In the present chapter, we discuss the current knowledge of correlates of protection and vaccine strategies.