Immunological infertility

Abstract

Immunological infertility is the presence, in one or both partners, of an antisperm immune reaction capable of interfering with fertility variables. In about 8–10% of these couples the immunological phenomenon is on the male side, causing ‘male immunological infertility’ (1). Since the first demonstration that a significant number of infertile men show an autoimmunity to sperm, experiments have suggested that antisperm antibodies (ASA) can interfere with the fertilizing ability of spermatozoa (2). ASA can act negatively on the motility of spermatozoa in semen, on their ability to pass through female genital secretions, or on the penetration of the oocyte. In particular, owing to in vitro fertilization techniques, it has been possible to demonstrate the effects of antibody-bound sperm directly, at the level of in vitro gamete interaction (3). ASA can reduce the motility and concentration of spermatozoa, and can induce sperm agglutination. However, normozoospermia can be accompanied by a high percentage of antibodies bound to the sperm surface, or a high ASA titre in serum or seminal plasma. In addition, ASA can affect sperm penetration of cervical mucus. When ASA are present in cervical mucus or bound to the sperm surface, impaired sperm penetration of cervical mucus, and abnormal swimming behaviour within cervical mucus—ranging from complete immobilization of sperm, to vibratory motion with limited progression (‘shaking reaction’), to restricted tail beat frequency and loss of rotatory motion—may be observed during the post-coital test (PCT). The shaking reaction in these cases is presumably due to cross-linking of motile, antibody-coated spermatozoa to the cervical mucus gel via the Fc part of the antibody (4). ASA may also inhibit fertilization by binding specifically to membrane antigens involved in sperm–oocyte interaction. They can additionally impair the fertilization process at the levels of the acrosome reaction, of zona pellucida recognition and penetration, and of sperm–vitellus interaction (5).