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Updated: Oct 14, 2025
Phenotypic and Functional Analysis of Activated Regulatory T Cells Isolated from Chronic Lymphocytic Choriomeningitis Virus-infected Mice
Published on: June 22, 2016
Characterization of Pathogenic CD8+ T cells in Chlamydia-Infected OT1 Mice
Zengzi Zhou1,2, Qi Tian3, Luying Wang1
1The 3rd Xiangya Hospital, Central South Universitygrid.216417.7, Changsha, Hunan, China.
Abstract:
Chlamydia trachomatis is a leading infectious cause of infertility in women due to its induction of lasting pathology such as hydrosalpinx. Chlamydia muridarum induces mouse hydrosalpinx because C. muridarum can both invade tubal epithelia directly (as a first hit) and induce lymphocytes to promote hydrosalpinx indirectly (as a second hit). In the current study, a critical role of CD8+ T cells in chlamydial induction of hydrosalpinx was validated in both wild type C57BL/6J mice and OT1 transgenic mice. OT1 mice failed to develop hydrosalpinx partially due to the failure of their lymphocytes to recognize chlamydial antigens. CD8+ T cells from naive C57BL/6J mice rescued the ability of recipient OT1 mice to develop hydrosalpinx when naive CD8+ T cells were transferred at the time of infection with Chlamydia. However, when the transfer was delayed for 2 weeks or longer after the Chlamydia infection, naive CD8+ T cells no longer promoted hydrosalpinx. Nevertheless, CD8+ T cells from mice immunized against Chlamydia still promoted significant hydrosalpinx in the recipient OT1 mice even when the transfer was delayed for 3 weeks. Thus, CD8+ T cells must be primed within 2 weeks after Chlamydia infection to be pathogenic, but, once primed, they can promote hydrosalpinx for >3 weeks. However, Chlamydia-primed CD4+ T cells failed to promote chlamydial induction of pathology in OT1 mice. This study optimized an OT1 mouse-based model for revealing the pathogenic mechanisms of Chlamydia-specific CD8+ T cells.
Insights
Chlamydia muridarum causes infertility via hydrosalpinx. CD8+ T cells are crucial for this pathology, but must be primed within two weeks of infection to promote lasting damage.
Area of Science:
- Immunology
- Microbiology
- Reproductive Health
Background:
- Chlamydia trachomatis is a major cause of female infertility, often leading to hydrosalpinx.
- Chlamydia muridarum induces hydrosalpinx in mice through direct invasion and immune-mediated damage.
- The role of specific T cell subsets in Chlamydia-induced pathology requires further elucidation.
Purpose of the Study:
- To investigate the critical role of CD8+ T cells in Chlamydia muridarum-induced hydrosalpinx.
- To determine the optimal timing for CD8+ T cell priming to induce pathogenic effects.
- To establish an optimized OT1 mouse model for studying Chlamydia-specific CD8+ T cell pathogenicity.
Main Methods:
- Utilized wild-type C57BL/6J and OT1 transgenic mice for Chlamydia muridarum infection models.
- Performed adoptive transfer of naive and Chlamydia-primed CD8+ T cells into OT1 mice at various time points post-infection.
- Assessed the development of hydrosalpinx as a measure of Chlamydia-induced pathology.
Main Results:
- OT1 mice, lacking Chlamydia-specific T cell recognition, showed reduced hydrosalpinx development.
- Transfer of naive CD8+ T cells rescued hydrosalpinx development when administered concurrently with infection.
- Delayed transfer of naive CD8+ T cells (≥2 weeks) failed to promote hydrosalpinx, while primed CD8+ T cells remained pathogenic even after 3 weeks.
- CD4+ T cells did not contribute to Chlamydia-induced hydrosalpinx in this model.
Conclusions:
- CD8+ T cells are essential for Chlamydia-induced hydrosalpinx.
- Effective CD8+ T cell pathogenicity requires priming within two weeks of Chlamydia infection.
- Once primed, CD8+ T cells can mediate hydrosalpinx for over three weeks.
- The study refined an OT1 mouse model for dissecting the pathogenic mechanisms of Chlamydia-specific CD8+ T cells.
