Thirty-six infertile couples underwent treatment by in-vitro fertilization. In 16 couples (group 1) the male partner was positive for antisperm antibodies measured by direct mixed antiglobulin reaction, direct immunobead test, and serum and/or seminal plasma tray agglutination test. In 20 couples (group 2) the men had no such antibodies. Men with poor sperm motility were excluded. The female partners had no antisperm antibodies, and in the controls (group 2) infertility was due to a known female factor. The fertilization rate in couples without antisperm antibodies (group 2) was 72.7% compared to 50.5% when the men had antibodies. However, the pregnancy rate per embryo transfer was not significantly different in the two groups (46.1% in group 1, 33.3% in group 2). This indicates that antisperm antibodies in the male interfere with sperm--egg fusion and subsequent fertilization but once fertilization has occurred, the pregnancy rate remains the same.

In 168 azoospermic males with normal or only slightly raised serum FSH levels, serum antisperm antibodies were measured, and the site of obstruction or the nature of the failure of spermatogenesis was defined by exploratory scrototomy with inspection of epididymes, vasography and testicular biopsy. When possible, surgical reconstruction was done by side-to-side epididymovasostomy, with vasovasostomy when necessary using 6/0 Prolene and no splints. Acquired blocks of cauda epididymis (34 cases) and vas (23 cases) were significantly more commonly associated with serum antisperm antibodies than congenital bilateral absence of vasa (29 cases) or blocks at the caput epididymis (48 cases), most of which were associated with sinusitis, bronchitis or bronchiectasis (Young's syndrome). Many of the former patients came from abroad, whereas most of the latter came from the British Isles. Sperm counts of 10 million per ml or more were produced by 23 (45%) of 51 adequately followed up patients with acquired blocks following surgical reconstruction, and 11 pregnancies (21.5%) were produced. Amongst those with spermatozoa in the ejaculate after surgery, serum antisperm antibodies were found significantly less often in those whose wives became pregnant compared with those who failed to produce pregnancies. It is concluded that failure of surgical treatment in some of these cases may have an immunological basis. No success was achieved with other groups.

Antisperm antibodies have been found in about 8% of men with infertility and in 60 to 80% of patients following vasectomy. In order to investigate the way antibodies influence sperm function we studied serum and seminal plasma from patients with infertility (n = 61) or undergoing vasovasostomy (n = 25). These antisera were characterised to determine their TAT titre, the nature of the target antigens and their capacity to interfere directly with fertilisation. The results indicate that antibodies from both groups of patients exhibit a capacity to stimulate or suppress sperm/oocyte fusion. The proportion of samples showing stimulatory activity was higher (50%) in the vasovasostomised population than in patients with infertility (21%). The remainder of the antisera suppressed sperm/oocyte fusion. There was no correlation between the titre of antisperm antibodies and their capacity to influence sperm function, indicating that it is the nature of the target antigens which is of significance rather than the antibody concentration. Western blot analysis indicated that these antisera targeted a group of sperm surface antigens with molecular weights of 30kD (35,45,66,90 and 115kD). Monoclonal antibodies are now being prepared in order to determine which of these specific components are involved in the suppression of sperm function.