Role of cell-mediated immunity in chlamydial infection: implications for ocular immunity.

Abstract

Cellular immunity to Chlamydia trachomatis is not well understood. Studies with the mouse pneumonitis agent in a mouse pneumonia model suggest a strong thymic component to immunity and a role for the macrophage as an effector cell in cell-mediated immunity to C. trachomatis. Experiments with Chlamydia psittaci indicate that cellular cytotoxic mechanisms and biostatic or cytotoxic mechanisms involving cytokines may also play a role in host defense against chlamydiae. Interferon has been shown to inhibit intracellular growth of both C. trachomatis and C. psittaci in vitro. Further studies are needed on the role of T lymphocytes or lymphokines and macrophages in limiting the growth of C. trachomatis in conjunctival epithelial cells (the most appropriate target cells) and in exerting a toxic effect on these cells. The evidence suggests that macrophages are activated during C. trachomatis infection; this activation may lead to the release of monokines (such as interleukin 1) that may be important in the pathogenesis of scarring due to over-stimulation of cellular immunity during ocular infection. Cell-mediated immunity to ocular infection with C. trachomatis may thus be a double-edged sword.