The production of antisperm antibodies (ASA) can occur in the male and/or in the female. In the male, it is due to a disruption in the blood-testis barrier that brings the sperm inside the testicle into contact with blood antibodies. In the female, it is thought to be due to damage to the wall of the genital tract that allows the presence of AAEs primarily in the cervical mucus.
These AAE can cause decreased sperm motility, or agglutination of sperm, as well as molecular damage that prevents fertilization or produces altered embryonic development.
As for treatment, corticosteroids were positioned as the first therapeutic step since they improved sperm quantity and motility, although their efficacy in increasing the number of gestations was doubtful. It seems that artificial insemination with or without corticosteroids improves the possibility of gestation, but it is IVF that achieves the highest pregnancy rates, and is the main therapeutic option for women with the presence of ESA.