Autoimmune premature ovarian failure.

Abstract

Premature ovarian failure (POF) may be caused by a variety of factors that result in the depletion of responsive ovarian follicles. There is a increasing body of evidence that suggests an autoimmune etiology in some POF patients. Data in support of an autoimmune etiology include: (1) lymphocytic and plasma cell infiltration of the ovary and alteration of T cell subsets; (2) circulating autoantibodies to ovarian antigens; (3) association with other "autoimmune" disorders; (4) recovery of ovarian function after regression of autoimmune status. The mechanism for ovarian autoimmunity is unknown. Genetic or environmental factor might be involved in the stimuli inducing immune response. The possibility that major histocompatibility complex antigen and cytokines are implicated in human autoimmune POF has been proposed. The relative contribution of cell-mediated immunity and antibody-mediated immunity remains obscure in animal models and in POF patients. Currently, in vitro fertilization and/or gamete intrafallopian transfer with donated oocytes are the best therapeutic options to achieve pregnancy although ovulation induction and immunosuppressive treatment might be used in approved experimental protocols. A newly developed double bridged enzyme linked immunosorbent assay (ELISA) might be useful in screening POF patients to identify those for whom temporary treatments may improve fertility.