Th2 Cells and Th17 Cells in the Development of Endometriosis – Possible Roles of Interleukin-4 and Interleukin-17A

Yutaka Osuga, Yasushi Hirota, Tetsuya Hirata, Masashi Takamura, Yoko Urata, Miyuki Harada, Gentaro Izumi, Tomoyuki Fujii, Kaori Koga
In: Journal of Endometriosis and Pelvic Pain Disorders · 2016 · vol. 8(4) , pp. 136–140 · doi:10.5301/je.5000257 · W2554985398
article OA: closed CC0 ⤵ 10 in-corpus citations
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Th2 and Th17 cells secrete IL-4 and IL-17A respectively, which promote endometriosis development by inducing cell proliferation, inflammation, and estrogen production.

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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.

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endometriosis

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