Antisperm antibodies: Fact or fiction? A personal account

This article has provided historical information concerning how immunities to sperm can alter human reproductive function. It has not provided proof that ASA cause infertility. It should be clear to the reader that ASA have the potential to delay conception. The accumulated evidence from laboratory-based studies provides strong circumstantial evidence that immunities to spermatozoa can potentially impair the entry of sperm into the female reproductive tract, shorten their longevity therein, and alter processes leading to fertilization. There are no prospective studies that demonstrate a decreased fecundity among couples in whom ASA is detected compared with couples without sperm immunities. Although we have maintained that such studies are needed as proof of immunologic infertility, such data are not likely to be available in the near future. Given the low incidence of significant immunities to sperm in men and women (approximately 3-5% of the infertile population), many centers will be needed to participate in a prospective study of the effects of ASA on fertility, and patient acquisition will be slow. In addition, in our retrospective analysis of pregnancies in women treated for infertility, husbands who exhibited an autoimmunity to sperm but were not themselves treated achieved pregnancy rates that varied from 15.3% to 66.7%, depending on the proportion of spermatozoa coated with immunoglobulin. These results suggest that a large number of subjects will be needed in order to detect differences in fertility between antibody-positive and antibody-negative groups. Currently used tests, whether Immunobead binding or MAR, do not identify the sperm-associated antigens to which ASA are directed. Antibodies directed against different antigens would be expected to play differing roles in impairing processes leading to successful fertilization, and this appears to be the case. When transferred to sperm of known fertile men, ASA detected in sera of infertile couples have varying effects on gamete interactions in vitro, as judged by both hemizona assay and sperm penetration of zona-free hamster eggs. It is difficult to select homogenous groups of couples with immunities to sperm for study. For these reasons, a prospective analysis of pregnancy rates of men or women with immunities to sperm is not currently feasible. I would argue, however, that one need not wait for indisputable clinical proof that ASA can cause infertility to recommend treatment. Sufficient circumstantial evidence exists that antibodies directed against sperm can alter sperm function. Tests should be performed for their presence, and if detected, effective treatment recommended.