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Interleukin 17 receptor E identifies heterogeneous T helper 17 cells in peritoneal fluid of severe endometriosis patients
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  • Yanping Jiang,
  • Lu Wang,
  • Yaqin Peng,
  • Jian Qin,
  • Aili Tan,
  • Shujun Wang
Yanping Jiang
Renmin Hospital of Wuhan University

Corresponding Author:[email protected]

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Lu Wang
Renmin Hospital of Wuhan University
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Yaqin Peng
Renmin Hospital of Wuhan University
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Jian Qin
Renmin Hospital of Wuhan University
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Aili Tan
Renmin Hospital of Wuhan University
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Shujun Wang
Renmin Hospital of Wuhan University
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Abstract

Endometriosis is a chronic inflammatory disorder resulting in pelvic pain and infertility. The role of T helper 17 (Th17) cells in endometriosis remains elusive. In this study, through detecting CXCR3, CCR4, CCR10, CCR6, interleukin-17 Receptor E (IL-17RE), and CD27, live RORγt-and-IL-17A-expressing Th17 cells were distinguished and sorted from peritoneal fluid (PF) of patients with stage III and IV endometriosis. Furthermore, we found that IL-17RE and CD27 were the labels of heterogeneous PF Th17 subsets, i.e. IL-17RE-CD27- subset, IL-17RE+CD27- subset, and IL-17RE+CD27+ subset. The former two subsets expressed higher IL-17A, GM-CSF, and IL-22 and were more proliferative than the latter subset. RNA-Seq analysis on IL-17RE+ Th17 subset and IL-17RE- Th17 subset revealed up-regulation of genes involved in oxidative phosphorylation and electron transport chain in IL-17RE+ Th17 subset relative to IL-17RE- Th17 subset. Consistently, the IL-17RE+ Th17 subset produced more adenosine triphosphate (ATP) and reactive oxygen species (ROS) than IL-17RE- Th17 subset. In conclusion, this study provides a novel method to detect and isolate live PF Th17 cells from endometriosis patients and unveils the functional and metabolic heterogeneity of PF Th17 subsets. Therefore, it sheds light on the elucidation of molecular mechanisms that modulate the function of pathological Th17 cells in endometriosis.
30 Jun 2021Submitted to Clinical & Experimental Immunology
27 Jul 2021Submission Checks Completed
27 Jul 2021Assigned to Editor
27 Jul 2021Reviewer(s) Assigned