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Th2 cells and Th17 cells in the development of endometriosis – possible roles of interleukin-4 and interleukin-17A

Th2 cells and Th17 cells in the development of endometriosis – possible roles of interleukin-4 and interleukin-17A

J Endometr Pelvic Pain Disord 2016; 8(4): 136 - 140

Article Type: REVIEW

DOI:10.5301/je.5000257

Authors

Yutaka Osuga, Yasushi Hirota, Tetsuya Hirata, Masashi Takamura, Yoko Urata, Miyuki Harada, Gentaro Izumi, Tomoyuki Fujii, Kaori Koga

Abstract

Endometriosis is recognized as an inflammatory disease in which inflammatory cytokines, such as interleukin (IL)-1β and TNFα, play important roles. Immunological factors are also suggested to be involved in the pathogenesis of endometriosis. This review provides comprehensive knowledge about helper T cell (Th cell) and its specific cytokines in endometriosis. A series of our studies demonstrated the presence of Th2 cells and Th17 cells in endometriotic tissues and revealed multiple effects of IL-4 and IL-17A, cytokines secreted from respective Th cells. IL-1β induces secretion of thymic stromal lymphopoietin (TSLP), a regulator for differentiation of inflammatory Th2 cells, in endometriotic stromal cells (ESCs). IL-4 stimulates proliferation of ESCs and production of 3β-hydroxysteroid dehydrogenase Type 2, an enzyme in an estrogen production pathway, in ESCs. IL-17A stimulates IL-8 and Gro-α secretion from ESCs and proliferation of ESCs. IL-17A-induced Gro-α promotes neutrophil migration, which may contribute to the presence of neutrophils in endometriotic tissues. IL-17A also increases secretion of CCL20, a chemokine for Th17 cells, from ESCs, which seems to induce migration of Th17 cells to the endometriotic tissues and enhance the effects of IL-17A further. TNFα in combination with IL-17A synergistically enhances secretion of IL-8 and CCL-20, suggesting cooperation of inflammation and Th17 immune response. These findings suggest that IL-4 and IL-17A promote the development of endometriosis through induction of cell proliferation, inflammation, and estrogen production. It is thus also suggested that IL-4 and IL-17A would be a target of treatment of the disease.

Article History

Disclosures

Financial support: This work was supported by grants in aid for Scientific Research from the Ministry of Health, Labour, and Welfare and Ministry of Education, Culture, Sports, Science and Technology and by grants from the Japan Agency for Medical Research and Development.
Conflict of interest: None of the authors has financial interest related to this study to disclose

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Authors

Affiliations

  • Department of Obstetrics and Gynecology, Graduate School of Medicine, The University of Tokyo, Tokyo - Japan

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