4.7 Article

Differential Levels of Regulatory T Cells and T-Helper-17 Cells in Women With Early and Advanced Endometriosis

Journal

JOURNAL OF CLINICAL ENDOCRINOLOGY & METABOLISM
Volume 104, Issue 10, Pages 4715-4729

Publisher

ENDOCRINE SOC
DOI: 10.1210/jc.2019-00350

Keywords

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Funding

  1. Japan Society for the Promotion of Science (JSPS) [24592474, 15K10675]
  2. Grants-in-Aid for Scientific Research [15K10675] Funding Source: KAKEN

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Context: Regulatory T (Treg) cells and T-helper-17 (Th17) cells may be involved in endometriosis. Information on the pattern of change in the percentages of Treg and Th17 cells in the peripheral blood (PB) and peritoneal fluid (PF) of women with early and advanced endometriosis is unclear. Objective: To investigate the pattern of change in the percentages of Treg and Th17 cells in the PB and PF of women with early and advanced endometriosis. Methods: We recruited 31 women with laparoscopically and histologically confirmed, revised American Society of Reproductive Medicine stage I-II endometriosis, 39 women with stage III-IV endometriosis, and 36 control subjects without visible endometriosis. PB and PF samples were collected and T-cell subpopulations analyzed by flow cytometry using specific monoclonal antibodies recognizing CD4(+), CD25(+), FOXP3(+), and IL-17A(+) markers. PF concentrations of TGF-beta and IL-17 were measured by ELISA. Results: The percentages of CD25(+) FOXP3(+) Treg cells within the CD4(+) T-cell population were significantly higher in the PF of women with advanced endometriosis than in either early endometriosis or in control subjects (P < 0.05 for both). A persistently lower percentage of CD4(+) IL-17A(+) Th17 cells was found in both PB and PF of women with early and advanced endometriosis. Compared with IL-17 levels, PF levels of TGF-beta were significantly higher in women with endometriosis (P = 0.01). Conclusion: Our findings reconfirmed the current speculation that endometriosis is related to alteration of Treg and Th17 cells in the pelvis causing survival and implantation of ectopic endometrial lesions.

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