CYTOTOXIC-T-LYMPHOCYTE-MEDIATED CYTOLYSIS OF L-CELLS PERSISTENTLY INFECTED WITH CHLAMYDIA SPP

Persistent chlamydial infections have been proposed as a means whereby chlamydiae evade immune resolution of infection. Such a mechanism wou ld require evasion not only of the humoral immune responses but also o f cell-mediated immune responses. We hypothesized that if such a mecha nism is important, persistently infected cells should not be recognize d by cytotoxic T cells. Persistent infections were simulated in vitro by treatment of Chlamydia trachomatis- or Chlamydia psittaci-infected cells with gamma interferon (IFN-gamma), penicillin, or tryptophan dep letion. Cultures were examined for induction of a chlamydial stress re sponse (measured by transcription of groesl RNA) and for the effects o n viability, infectivity, morphology, and immune recognition. Although both IFN-gamma and penicillin induced aberrant chlamydial morphology and growth, we did not find evidence that these treatments elicited a classical stress response. In addition, T-cell-mediated lysis of Chlam ydia-infected target cells treated with IFN-gamma or penicillin or gro wn in tryptophan-deficient media was examined. The immune cell-mediate d lysis of these treated infected cells demonstrated that despite the effects of these compounds on chlamydial growth and development, the i nfected cells continued to be efficiently recognized and killed by cyt otoxic T cells. Thus, it seems unlikely that these in vitro models of persistence represent functional mechanisms to evade immune clearance.