Effects of human antisperm antibodies on development of preimplantation embryos.

The effects of antisperm antibodies (ASAs) present in sera of immunoinfertile patients and vasectomized men were investigated on preimplantation embryonic development in mice. Of the nine immunoinfertile sera tested, two were effective in inhibiting blastulation rates of in vitro cultured murine 2-cell embryos (p less than .05 to .002). Similarly, sera from two of the three vasectomized men were capable of affecting early embryonic development in mice (p less than .05 to .002). Specificities of the embryotoxic effects of ASAs were further confirmed by culturing embryos in the presence of affinity-purified monovalent Fab' antibodies isolated from these sera. Fab' antibodies from only one of the two immunoinfertile patients whose sera affected blastulation rates, and from one of the three vasectomized men were effective in influencing blastulation rates of in vitro cultured 2-cell murine embryos (p less than .05 to .001), mainly due to an arrest of development at 2 to 8-cell and morula stages. In the Western blot procedure, none of the immunoinfertile Fab' antibodies recognized any specific band on blots of extracts from murine ova or 2-cell embryos. However, all the immunoinfertile Fab', but not fertile control Fab', specifically recognized a protein band in the M(r) 25 +/- 2 kD region, on the Western blots of extract from murine blastocyst stage embryos. In addition, Fab' from one immunoinfertile serum, which inhibited embryonic development, reacted specifically with a protein band in the lower molecular range (approximate M(r) 12 kD) on Western blot involving exact from blastocysts. Fab' antibodies of sera from vasectomized men did not react with any specific protein band on blots of extracts from murine ova, 2-cell embryo, or blastocyst. These results suggest that ASAs from some immunoinfertile patients and vasectomized men, especially those reacting with 12-kD blastocyst protein, are capable of affecting preimplantation embryonic development in mice, and thus may contribute toward immunologically medicated infertility both at fertilization and postfertilization stages.