Suppression of chlamydial pathogenicity by nonspecific CD8+t lymphocytes

Lingxiang Xie, Conghui He, Jianlin Chen, Lingli Tang, Zhiguang Zhou, Guangming Zhong

Research output: Contribution to journalArticlepeer-review

4 Scopus citations

Abstract

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 (OVA457-462). 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 OVA457-462 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.

Original languageEnglish (US)
Article numbere00315
JournalInfection and immunity
Volume88
Issue number10
DOIs
StatePublished - Oct 2020

Keywords

  • CD8T cells
  • Chlamydia
  • Hydrosalpinx
  • Pathogenesis
  • Suppression
  • Tregs

ASJC Scopus subject areas

  • Infectious Diseases
  • Parasitology
  • Microbiology
  • Immunology

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