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Anti-sperm Antibodies and their Significance

The immune system recognizes self from non-self. Proteins present on plasma membranes, lipids, nucleic acids, and polysaccharides act as antigens. Antigens present during fetal life are presented to the thymus gland and tolerance to them develops. Antigens presented later in life which are recognized as foreign have antibodies produced against them and the cells bearing these antigens are ultimately destroyed. The testes are immunologically privileged with several mechanisms present to keep the systemic immune system separate, as will be discussed below. Perturbations of these may lead to recognition of antigens in the testes and antibody formation. Sperm are not produced until after puberty so may be seen as foreign. Immunoglobulins are antibodies produced in response to a specific antigen. There are 5 different classes, three of which appear to be involved with ASA. IgM is a pentamer weighing 900 kD; IgG is a monomer weighing 150 kD, and IgA is either a monomer or dimer between 150 kD and 400 kD. IgA is secreted in bodily secretions, including cervical mucus (1), seminal vesicles, prostate, bulbourethral and urethral glands, and epididymis (2). IgG and IgM (least common) are present in serum and appears in semen as a transudate.

The presence of a blood-testis barrier prevents the development of sperm autoimmunity by sequestering the germ cells in the testes away from the systemic immune system. This is due to tight junctions between Sertoli Cells and the inability of macromolecules to enter the seminiferous tubule lumen. It is possible that obstruction of sperm egress via blockade of the outflow (i.e. vasectomy) causes the blood-testis barrier to break down. This may occur in men with congenital absence of the vas deferens (CAVD), traumatic obstruction, unilateral focal cryptic obstruction at the level of the seminiferous tubules may lead to ASA formation (3). The barrier may not be complete, particularly at the level of the rete testis. Prelepotene germ cells in the basement compartment of the seminiferous tubule are accessible to circulating antibodies and are immunogenic. Sertoli cells appear to produce an anti-lymphocytic activity, which may help buffer this breach in the barrier. Thus, Sertoli Cells may contribute the maintenance of immune privilege. Studies have suggested that FasL is expressed on Sertoli Cells and may be involved with maintenance of immune privilege by inducing apoptosis of Fas expressing T Lymphocytes (4). Hence, several mechanisms may play a role in the production of ASA.

ASA increase sperm agglutination in semen analysis. ASA IgA inhibits penetration of cervical mucus and migration and ASA may inhibit the loss of cholesterol required for the capacitation of sperm (5). Of course, ASA may block binding to the zona pellucida and inhibit fertilization (6). Cognate sperm antigen (SAGA-1) is identical to the lymphocyte surface glycoprotein CD52 (7) indicating the importance of membrane glycoproteins in ASAs. While ASA may play a role in male infertility, diverse methods of assessment make comparisons difficult, but 15 % of patients may be affected (1).

References:

1. Mazumdar S, Levine A. Antisperm antibodies: etiology, pathogenesis, diagnosis, and treatment. 1998. Fertility and Sterility 70(5):799-810.

2. Jequier A. Infertility and the presence of antisperm antibodies. In Male Infertility; A Guide for the Clinician. 2000 Blackwell Science, London, pp274-287.

3. Bronson R. Antisperm antibodies: a critical evaluation and clinical guidelines. 1999. J. Reproduct. Immunol. 45:159-183.

4. Filippini A, Riccioli A, Pasula F, Lauretti P, D’Alessio A, Cesaris P, Gandini L, Lenzi A, Ziparo E. Immunology and immunopathology opf the male genital tract; control and impairment of immune privilege in the testis and semen. 2001. Human Repro. Update. 7(5):444-449.

5. Bates CA. Antisperm antibodies and male subfertility. 1997. Br. J. Urol. 80: 691-97.

6. Sibharata H, Shiraishi Y, Hirano Y, Suzuki T, Takamizawa S, Suzuki M. Diversity of the inhibitory effects on fertilization by anti-sperm antibodies bound to the surface of ejaculated sperm. 2003. Hum. Repro. 18(7):1469-73.

7. Diekman AB, Norton EJ, Westbrook VA, Klotz KL, Naaby-Hansen S, Herr JC. Anti-sperm antibodies from infertile patients and their cognate sperm antigens: a review. Identity between SAGA-1, the H6-3C4 antigen, and CD52. 2000 AJRI 43:134-43.
 

 

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