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Molecular Pathogenesis

Suppression of Chlamydial Pathogenicity by Nonspecific CD8+ T Lymphocytes

Lingxiang Xie, Conghui He, Jianlin Chen, Lingli Tang, Zhiguang Zhou, Guangming Zhong
Craig R. Roy, Editor
Lingxiang Xie
aDepartment of Microbiology, Immunology and Molecular Genetics, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA
bThe Second Xiangya Hospital of Central South University, Changsha, Hunan, China
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Conghui He
aDepartment of Microbiology, Immunology and Molecular Genetics, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA
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Jianlin Chen
bThe Second Xiangya Hospital of Central South University, Changsha, Hunan, China
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Lingli Tang
bThe Second Xiangya Hospital of Central South University, Changsha, Hunan, China
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Zhiguang Zhou
bThe Second Xiangya Hospital of Central South University, Changsha, Hunan, China
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Guangming Zhong
aDepartment of Microbiology, Immunology and Molecular Genetics, University of Texas Health Science Center at San Antonio, San Antonio, Texas, USA
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Craig R. Roy
Yale University School of Medicine
Roles: Editor
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DOI: 10.1128/IAI.00315-20
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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.

FOOTNOTES

    • Received 26 May 2020.
    • Returned for modification 15 June 2020.
    • Accepted 27 July 2020.
    • Accepted manuscript posted online 3 August 2020.
  • Supplemental material is available online only.

  • Copyright © 2020 American Society for Microbiology.

All Rights Reserved.

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Suppression of Chlamydial Pathogenicity by Nonspecific CD8+ T Lymphocytes
Lingxiang Xie, Conghui He, Jianlin Chen, Lingli Tang, Zhiguang Zhou, Guangming Zhong
Infection and Immunity Sep 2020, 88 (10) e00315-20; DOI: 10.1128/IAI.00315-20

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Suppression of Chlamydial Pathogenicity by Nonspecific CD8+ T Lymphocytes
Lingxiang Xie, Conghui He, Jianlin Chen, Lingli Tang, Zhiguang Zhou, Guangming Zhong
Infection and Immunity Sep 2020, 88 (10) e00315-20; DOI: 10.1128/IAI.00315-20
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KEYWORDS

Chlamydia
pathogenesis
hydrosalpinx
CD8+ T cells
Tregs
suppression

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