Chapter 8 : Human Immunity to Chlamydiae

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This chapter addresses the question of and data for natural immunity to chlamydial infection, focusing on data on infections in humans. It summarizes the limited information on immunity to human infection, and discusses the basis of individual susceptibility to chlamydial infection and disease with reference to chlamydial immunity. The relationships between determinants for host susceptibility to infection, persistence of infection, and propensity to cause disease are highlighted in this chapter. The chapter also discusses of the role that immune evasion mechanisms have on interventions such as vaccines. Chlamydiae are surprisingly susceptible to inactivation by humoral and cellular innate defenses. Results from several observations suggested that major outer membrane protein (MOMP)-specific T CD4 T cells are important in immunity to infection and disease and that Hsp60-specific T-like CD4 T cells are associated with the pathological sequelae of persistent chlamydial infection. The authors suggest that Fc-receptor-mediated cell entry enhanced susceptibility to chlamydial infection. A complex web of host and pathogen determinants appears to constrain the outcome of chlamydial infection. Infection with induces strong serum antibody responses. At the population level, serum antibodies are principally acquired between ages 5 and 14 years, with approximately 50 to 75% of adults having antibody to . Both peripheral blood and synovial fluid mononuclear cells have been successfully used in lymphoproliferation assays.

Citation: Brunham R. 1999. Human Immunity to Chlamydiae, p 211-238. In Stephens R (ed), Chlamydia. ASM Press, Washington, DC. doi: 10.1128/9781555818203.ch8
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Table 1

Association of submucosal lymphoid follicle formation with l cervicitis and endometritis

Citation: Brunham R. 1999. Human Immunity to Chlamydiae, p 211-238. In Stephens R (ed), Chlamydia. ASM Press, Washington, DC. doi: 10.1128/9781555818203.ch8

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