Figure 1.
The role of IL-17 in endometriosis. Increased IL-17 in PF, serum, endometriotic lesions and etc. leads to the proliferation, invasion and implantation of ectopic endometrium partly by recruiting and activating neutrophil and M2 macrophage. And the macrophage secretes NOS2 and NO, giving rise to co-existence of endometriosis and infertility. IL-17 also acts directly on its own and indirectly through IL-8. The promotion of vasculogenesis and angiogenesis is another important role of IL-17, which can act through a variety of pathways, such as stimulation of vascular endothelial cell migration and cord formation, recruitment of lymphocytes and bone marrow-derived cells and inducing elaboration of a variety of proangiogenic factors (e.g., VEGF, IL-1β, TNF-α, and IL-8). Abbreviations: PF, peritoneal fluid; IL, interleukin; G-CSF, colony-stimulating factor; GM-CSF, granulocyte macrophage colony-stimulating factor; ROS, reactive oxygen species; VEGF, vascular endothelial growth factor; NOS2, nitric oxide synthase 2; NO, nitric oxide; Gro-α, growth-related oncogene-α; TNF-α, tumor necrosis factor-α; ESC, endometriotic stromal cell.