Immunological aspects of endometriosis.

During the past decade, evidence has accumulated indicating an association between endometriosis and changes in humoral and cell-mediated immunity. However, it is not clear whether immune changes are the sequelae or play a role in the etiopathogenesis of the disease. The latter concept is supported by the observation that exposure of rhesus monkeys to radiation or immunotoxicants leads several years later to an increase in frequency and severity of endometriosis. Studies from our laboratories support the theory that endometrial cells misplaced during menses can implant in ectopic locations only in women with genetically or environmentally altered cell-mediated immune function. Development of endometriosis may then prompt a humoral response in some women, which results in the production of autoantibodies to endometrial cells or cell-derived antigens. These autoantibodies may cross-react with the uterine endometrium, interfere with implantation, and cause infertility or early spontaneous abortions. We recently observed that the presence of autoantibodies in endometriosis was associated with significantly lower in vitro fertilization/embryo transfer pregnancy rates. Interestingly, in about 30% of women with unexplained infertility, immune changes characteristic of endometriosis were also present, suggesting a subclinical form of this disease. We conclude that: (1) women with unexplained infertility should have studies of the immune function to rule out subclinical form of endometriosis; (2) evaluation of infertility in women with endometriosis should include an assessment of autoantibody status; and (3) treatment methods involving autoantibody suppression should be considered in women with endometriosis positive for autoantibodies.