Suppression of Chlamydial Pathogenicity by Nonspecific CD8 + T Lymphocytes.

Chlamydia trachomatis , a leading infectious cause of tubal infertility, induces upper genital tract pathology, such as hydrosalpinx, which can be modeled with Chlamydia muridarum infection in mice. Following C. muridarum inoculation, wild-type mice develop robust hydrosalpinx, but OT1 mice fail to do so because their T cell receptors are engineered to recognize a single ovalbumin epitope (OVA _457-462 ). These observations have demonstrated a critical role of Chlamydia -specific T cells in chlamydial pathogenicity. In the current study, we have also found that OT1 mice can actively inhibit chlamydial pathogenicity. First, depletion of CD8 ⁺ T cells from OT1 mice led to the induction of significant hydrosalpinx by Chlamydia , indicating that CD8 ⁺ T cells are necessary to inhibit chlamydial pathogenicity. Second, adoptive transfer of CD8 ⁺ T cells from OT1 mice to CD8 knockout mice significantly reduced chlamydial induction of hydrosalpinx, demonstrating that OT1 CD8 ⁺ T cells are sufficient for attenuating chlamydial pathogenicity in CD8 knockout mice. Finally, CD8 ⁺ T cells from OT1 mice also significantly inhibited hydrosalpinx development in wild-type mice following an intravaginal inoculation with Chlamydia Since T cells in OT1 mice are engineered to recognize only the OVA _457-462 epitope, the above observations have demonstrated a chlamydial antigen-independent immune mechanism for regulating chlamydial pathogenicity. Further characterization of this mechanism may provide information for developing strategies to reduce infertility-causing pathology induced by infections.
(Copyright © 2020 American Society for Microbiology.)