Table 2.

Cytokines associated with the development of endometriosis.

Immune Factor	Role in Endometriosis
TNF-α	Increasing vascular permeability and transformation of inflammatory factors in the peritoneal cavity, which exacerbate peritonitis [66].
NF-κB	Controlling gene expression associated with immune response, cellular proliferation, and cytokine production [67].
MCP-1	Stimulation of monocytes to migrate from peripheral blood to the peritoneal cavity to turn into macrophages, leading to local inflammation [68].
IL-1β	Induction of VEGF and COX-2 expression leading to the progression of endometriosis [69].
IL-6	In the tide to impair the function of NK cells (natural killer) by regulating the protein expression of tyrosine phosphatase (SHP-2) in endometriosis [70].
IL-10	In a mouse model with induced endometriosis, inhibition of IL-10 activity was found to be helpful in reducing lesions [71].
IL-15	In normal endometrial cells, ovarian steroid hormones control the production of IL-15. Endometriotic cells in patients with endometriosis show higher concentrations of this cytokine in endometrial patients [72].
IL-16	Higher concentrations of IL-16 in women with endometriosis are associated with the development of the disease by stimulating the secretion of IL-6, TNF-α and IL-1β. IL-16 polymorphisms are associated with women’s susceptibility to the development of endometriosis and its severity [73].
IL-17A	In endometriosis, IL-17A is expressed in endometrial lesions, and therefore the inflammatory environment of the peritoneal cavity of patients with endometriosis may be associated with the production of IL-17A [74].
IL-18	IL-18 regulates the production of TNF-α and IL-8, acts as a potent angiogenic factor, and also regulates the intercellular expression of adhesion molecule 1 through NFκB and may increase MMP production. IL-18 is a major regulator of the immune response process in a wide range of cells that decreases in both eutopic and ectopic endometrium in endometriosis [75].
IL-27 IL-33	IL-10 + Th17 stimulate the proliferation and implantation of ectopic lesions and accelerate the progression of endometriosis, making IL-27 a key regulator in endometriotic lesions [76]. Member of the IL-1 family. IL-33 induces the synthesis of Th2-type cytokines through its orphan receptor ST2. Increased IL-33 expression has been correlated with fibrotic disorders such as skin scleroderma, liver and lung fibrosis, making IL-33 a key profibrotic mediator [77].
IL-37	Increased levels of IL-37 expression in eutopic and ectopic endometrium in women with stage III-IV ovarian endometriosis may be involved in inflammatory processes leading to endometriosis [78].