Endometriosis is characterized by the implantation and growth of endometriotic tissues outside the uterus. It is widely accepted the theory that
endometriosis is caused by the implantation of endometrial tissue from
retrograde menstruation; however,
retrograde menstruation occurs in almost all women and other factors are required for the establishment of
endometriosis, such as cell survival, cell invasion, angiogenesis, and cell growth.
Immune factors in the local environment may, therefore, contribute to the formation and progression of
endometriosis. Current evidence supports the involvement of immune cells in the pathogenesis of
endometriosis. Peritoneal neutrophils and macrophages secrete biochemical factors that help endometriotic cell growth and invasion, and angiogenesis. Peritoneal macrophages and NK cells in
endometriosis have limited capability of eliminating endometrial cells in the peritoneal cavity. An imbalance of T cell subsets leads to aberrant
cytokine secretions and
inflammation that results in the growth of
endometriosis lesions. It is still uncertain whether these immune cells have a role in the initial cause and/or stimulate actions that enhance disease; however, in either case, modulating the actions of these cells may prevent initiation or
disease progression. Further studies are needed to deepen the understanding of the pathology of
endometriosis and to develop novel management approaches of benefit to women suffering from this disease.