Autoantibodies in infertility: current opinion.

Abstract

The concept of autoimmune-related infertility has remained controversial. Traditionally, abnormal autoimmune function has been implicated as a contributing factor to female as well as male infertility. In the female, abnormal autoimmunity primarily relates to autoantibody activity against ovarian tissue components, whereas in the male, abnormal autoimmunity, believed to be clinically relevant, is mostly directed against the spermatozoon itself. Historically, abnormal autoimmune function has been seen as a rather organ-specific process in both female and male infertility, with either ovarian or testicular antigens as the primary targets. In recent years it has, however, also been recognized that additional, and possibly less organ-specific, processes of autoimmune nature may play a role. For example, female infertility patients have demonstrated a significantly higher incidence of nonorgan-specific autoantibody abnormalities. The incidence of such autoantibody abnormalities appears to be positively correlated to increasing intractability of infertility (Gleicher et al., 1993). On the other hand, there is doubt as to whether such non-organ-specific autoantibodies themselves cause disease or only serve as epiphenomena for a still undefined immunological defect which causes infertility (Gleicher, 1994). Lastly, the newly evolving field of neuroimmunology needs to be considered here. Since reproductive function is under neuroendocrine control, autoimmune processes that affect the hypothalamic–pituitary–gonadal axis at the central nervous system (CNS) level will have considerable impact on infertility. This review will therefore report on autoimmune abnormalities at CNS and gonadal levels and on non-organ-specific abnormalities systemically. It will also separate female from male findings since they are usually distinct, though both can often be found in a single couple presenting with an infertility problem.