Abstract: Endometriosis is a common female gynecological diseases, and it is histologically characterized by the displacement of endometrial tissue to extrauterine locations including the pelvic peritoneum, ovaries, and bowel. Dysmenorrhea, chronic pelvic pain, abnormal menstruation and infertility are the main symptoms, and the individual and global socioeconomic burden of endometriosis is significant. Laparoscopy remains the gold standard for the diagnosis of the condition. However, the invasive nature of surgery, coupled with the lack of a laboratory biomarker for the disease, results in a mean latency of 7-11 years from onset of symptoms to definitive diagnosis. Unfortunately, the delay in diagnosis may have significant consequences in terms of disease progression. The discovery of a high sensibility and specificity biomarker for the nonsurgical detection of endometriosis promises earlier diagnosis and prevention of deleterious sequelae and represents a clear research priority. The current pathogenesis is unknown. Immune factors and inflammatory responses have been reported to play an important role in the pathogenesis. Among them, the role of IL-16 in the pathogenesis of endometriosis has received increasing attention. IL-16 is a modulator of chemokine and T cell activation mediated by CD4 signaling. This article reviews the relationship between the expression of IL-16 and the pathogenesis of endometriosis.

Key words: Endometriosis, Interleukin-16, Inflammation, Polymorphism, genetic