Jun Fu, Ph.D., Yong Wang, Ph.D., Kin Lam Fok, Ph.D., Dantong Yang, Ph.D., Yi Qiu, Ph.D., Hsiao Chang Chan, Ph.D., Samuel S. Koide, Ph.D., M.D., Shiying Miao, Linfang Wang
Vol 97, Issue 5, Pages 1226-1233.e8
To show that antibodies against ACTL7a, a spermatozoon-specific protein, may be a cause of immunologic infertility.
Determine the presence of anti-ACTL7a antibodies in infertile blood, raise antibodies against ACTL7a in rabbits, and demonstrate that the in vitro treatment of mouse spermatozoa with infertile sera markedly reduces their fertilizing capacity. Demonstrate that the active immunization of mice with ACTL7a protein reduces fertility.
National Research Institute for Family Planning, Beijing, World Health Organization Collaboration Center of Human Reproduction, China.
Rabbits, ICR mice.
Main Outcome Measure(s):
Mass spectrometry, indirect immunostaining, spermatozoa agglutination test, and standard fertility assay.
The fertilizing potential of mouse spermatozoa was markedly reduced after in vitro treatment with ACTL7a antibody–containing serum from a vasectomized man. Active immunization with ACTL7a significantly reduced the fertility of mice. Anti-ACTL7a antibodies caused the agglutination of mouse and human spermatozoa in vitro. Furthermore, the antibodies were detected in the sera of additional vasectomized men.
Anti-ACTL7a antibodies may cause infertility in mice because the in vitro treatment of mouse spermatozoa with ACTL7a antibody–containing serum markedly reduced the fertilizing potential of the spermatozoa. In addition, the active immunization of mice with ACTL7a resulted in significant reductions in fertility.
Read the full text at: http://www.fertstert.org/article/S0015-0282(12)00257-9/fulltext