In women with endometriosis, the lining of the uterus, or endometrium, grows outside the uterus in the abdominal cavity. Those misplaced growths are called ectopic endometrium to distinguish them from the endometrium that grows correctly within the uterus (the eutopic endometrium). Endometriosis can cause pain and reduce fertility.
Although no one knows exactly why some women develop endometriosis, research has indicated that an altered immune response is involved. In particular, studies have pointed to a type of immune cell called a T regulatory cell, which suppresses the immune system, the body’s defensive mechanisms. T regulatory cells help maintain pregnancy by protecting the fetus from attack by the mother’s immune system. These cells also “hide” tumor cells from destruction by the immune system.
To learn about the relationship between T regulatory cells and the growth of endometrium, researchers funded by the Fertility and Infertility Branch worked with baboons, which have a menstrual cycle similar to that of humans. The researchers found that in baboons that developed endometriosis, the levels of T regulatory cells changed throughout the body. Compared to healthy baboons, the uterine (eutopic) endometrium of baboons with endometriosis contained fewer of these cells—a change that would reduce the baboons’ fertility.
The baboons with endometriosis also had more T regulatory cells in the ectopic endometrium compared to the levels found in eutopic endometrium of healthy animals, a change that could, protect the ectopic endometrial tissue from destruction by the body’s immune system, allowing the disease to continue.
The researchers found that receiving an abdominal operation early in the disease seemed to help the immune system begin to readjust to normal—regardless of whether that operation actually removed the endometriosis. These results are a step forward in understanding why endometriosis develops. They also provide more clues about effective surgical and immune-modifying treatments for the disorder (PMID: 22442246).