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Vasectomy

An experimental autoimmune disease state

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Ricerca in clinica e in laboratorio

Summary

Vasectomy, as an experimental autoimmune disease state in otherwise normal animals and humans, provides for the study of a variety of immunologic phenomena. These include: 1. the long-term effects of a continuous autoimmune response on various normal physiologic and immunologic processes; 2. the elucidation of the relationship between circulating antisperm antibodies and infertility underin vivo physiological conditions as well as at the molecular level; and 3. the genetic control of immune responsiveness to autologous sperm and testis antigens. The fact that only 50–60% of vasectomized subjects developed antisperm autoantibodies, regardless of the species studied, correlates with the finding that within a species, antisperm antibody responsiveness is strain-dependent. Furthermore, it has been shown by the use of a quantitative antibody assay that the postvasectomy IgG autoantibody response to sperm surface autoantigens (TSDA) in vasectomized GPs is controlled by a single dominant autosomal, or X-linked, gene. The development of postvasectomy autoimmune orchitis has been conclusively demonstrated in the GP and rabbit. In the GP, the onset of disease parallels the development of cell-mediated immune responsiveness to aspermatogenic antigens. Data fromin vitro fertilization experiments demonstrate that antisperm autoantibodies isolated from the sera of vasectomized GPs can essentially interfere with all prefertilization and fertilization events. Although the mechanism(s) and the nature of the molecules involved are unknown, these findings support the concept that serum antisperm autoantibodies present in vasovasostomized individuals may in part be responsible for the high rate of infertility following vasovasostomy. Autoantibodies present in the sera of vasectomized GPs react with three major radiolabelable sperm plasma membrane autoantigens of 69.62,000; 42,000 and 20,000 daltons. In addition to polypeptide autoantigens, autoantibodies in vasectomized GP sera react with an autoantigenic glycolipid(s) from GP testis and sperm. Finally, vasectomy appears to have a striking atherogenic effect in subhuman primates. The pathogenetic mechanism of postvasectomy atherosclerosis is likely to be the result of intimal injury, but the precise mechanism leading to such injuries is unknown. Although circulating sperm antigen-antibody complexes may be involved, to date the detection of such complexes does not appear to correlate with the development of postvasectomy atherosclerosis. An alternative hypothetical model based on the physical-chemical nature of some unusual sperm autoantigens has been presented. Glycolipid autoantigen(s) released from the testis after vasectomy may insert into the plasma membrane of endothelial cells, rendering these previously unsusceptible cells susceptible to immunologic injury by antisperm glycolipid autoimmune reactions. The attendant intimal injury may then lead to atherosclerosis, potentially the most serious complication of vasectomy.

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  1. Departments of Pathology and Biochemistry, University of New Mexico School of Medicine, 87131, Albuquerque, N. Mex., USA

    Cory Teuscher, Gaynor C. Wild, Edward Johnson & Kenneth S. K. Tung

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  1. Cory Teuscher
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  2. Gaynor C. Wild
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  4. Kenneth S. K. Tung
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Teuscher, C., Wild, G.C., Johnson, E. et al. Vasectomy. La Ricerca Clin. Lab. 11, 313–329 (1981). https://doi.org/10.1007/BF02909030

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