Tehran University of Medical Sciences

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Increased Circulating T Helper 17 (Th17) Cells and Endometrial Tissue Il-17-Producing Cells in Patients With Endometriosis Compared With Non-Endometriotic Subjects Publisher



Delbandi AA1, 7 ; Mahmoudi M2 ; Shervin A4 ; Farhangnia P3 ; Mohammadi T3 ; Zarnani AH5, 6
Authors

Source: Reproductive Biology Published:2025


Abstract

Endometriosis, an inflammatory disease, is characterized by the aberrant presence of endometrial tissues at ectopic locations. Accumulating evidence suggests that inflammatory cells, such as interleukin-17 (IL-17)-producing cells, may be involved in the pathogenesis of endometriosis. This investigation assessed the frequency of IL-17A (commonly known as IL-17)-producing cells in peripheral blood mononuclear cells (PBMCs), ectopic, and eutopic endometrial tissues in patients with endometriosis compared to non-endometriotic subjects. PBMCs, ectopic, and eutopic endometrial tissues were collected from 23 patients with endometriosis. PBMCs and endometrial tissues from 20 non-endometriotic women were used as the control group. The frequency of T helper 17 (TH17) lymphocytes in PBMCs was assessed using flow cytometry, and the expression level of IL-17 in eutopic and ectopic endometrial tissues was evaluated through immunohistochemistry. The percentage of TH17 and IL-17-producing lymphocytes was significantly higher in the PBMCs of patients with endometriosis compared to non-endometriotic subjects (P < 0.01 and P < 0.001, respectively). The expression of IL-17 protein in ectopic (P < 0.001) and eutopic (P < 0.05) endometrial tissues of patients with endometriosis increased compared to controls' endometrial tissue. Furthermore, the eutopic endometrium of patients with endometriosis showed a higher expression of IL-17 protein than the eutopic endometrial tissue of control subjects (P < 0.05). The findings suggest that the higher frequency of IL-17-producing cells in the PBMCs and endometrial tissues of patients with endometriosis contributes to the pathogenesis of endometriosis. © 2025 Society for Biology of Reproduction & the Institute of Animal Reproduction and Food Research of Polish Academy of Sciences in Olsztyn
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