Abstract: Endometriosis (EMs) is an estrogen-dependent disease, usually associated with chronic pelvic pain and infertility, affecting approximately 10% to 15% of women of childbearing age. In recent years, immune dysfunction has been shown to be a key factor in promoting the growth of ectopic lesions after endometrial debris retrograded. Almost all the immune cell functions in patients with EMs have changed, such as T cell reactivity and NK cell toxicity decrease, B cell polyclonal activation and antibody production increase, and the number of peritoneal monocytes increase. In addition, the high estrogen environment in EMs and the abnormal distribution of estrogen receptor subtypes have also been shown to affect the recruitment and function of immune cells. However, it is controversial whether immune dysfunction is the initial cause of EMs or the consequence of the disease.

Key words: Endometriosis, Immune system, Immunity, innate, Adaptive immunity, Immunity, cellular