Autoimmune premature ovarian failure: of mice and women

Autoimmunity is a well-established mechanism of premature ovarian failure and may be the dominant cause of reversible premature ovarian failure. Because of its strong analogy with the human disease, murine experimental post-thymectomy autoimmune oophoritis may provide insight into the pathogenesis of autoimmune premature ovarian failure in women and might open new avenues to specific diagnostic and therapeutic methods. We reviewed the literature on murine experimental post-thymectomy autoimmune oophoritis in order to compare and contrast it with human autoimmune premature ovarian failure, to which it is similar in several ways. The histologic distribution of the ovarian lymphocytic infiltration is similar, and both have reduced natural killer cell activity. Susceptibility appears to be associated with genes outside the major histocompatibility complex in both the mouse and the human. Finally, the mouse model disorder is associated with a persistent neonatal-like Th2 response, which suggests possible similarities with autoimmune polyglandular failure type 1 in humans. In this condition autoimmunity develops despite an impaired cellular immune response.