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Pathogenetical and Clinical Aspects of Antisperm Immunity

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Reproductive Immunology

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Abstract

Antisperm antibodies (ASA) have various possible levels of interference to impair the fertilizing capacity of human spermatozoa. In the semen, it has been demonstrated that ASA can induce the formation of spermagglutination and that they also have a negative effect on sperm motility and, after intra-vaginal ejaculation, on their ability to migrate through female genital secretions. ASA can also interfere with the fusion of the gametes, which is the key event of fecundation. The evidence suggests that ASA may inhibit fertilization by binding specifically to membrane Ag involved in the sperm-oocyte interaction. They can also inhibit zona pellucida recognition and penetration and the sperm-vitellus interaction as well as triggering a premature acrosome reaction. To date, ASA remain a serious and only partially understood factor that can compromise the success of the insemination and fertilization techniques used to treat infertility. Concerning male infertile patients, our data show a strict correlation between systemic and local immunization and between ASA presence in sera and bound on sperm surface. Furthermore, in our experience if specific Ig against sperm antigens bind to spermatozoa at a percentage higher than 70%, they they are able to interfere, in vivo, both with sperm-mucus interaction and sperm-utero-fallopian passage regardless of Ig class or site of the bond. In vitro, only the ASA bound to the acrosomal surface seem to prevent the sperm binding to the oocyte. As far as the immunosuppressive activity by human seminal plasma is due to multiple factors and reduced amount of these factors can contribute to the appearance of the ASA. Recent findings suggest that Fas ligand (FasL), expressed on the surface of Sertoli cells, is involved in maintaining the immune privilege by preventing activated lymphocytes from infiltrating the testis. The membrane-bound human FasL was found to be converted to a soluble from (sFasL) by the action of a matrix metalloproteinase-like. Human sFasL is a 26–35 kD glycoprotein and consists of the extracellular region of FasL which bind to Fas to induce apoptosis. It has been shown that activated human peripheral T cells accumulate FsL in the supernatant. These immunosuppressive activities have been proposed to play a role in the prevention of lymphocytes responses against sperm autoantigens in the male genital tract. In a recent experiment we studied 50 subjects—22 normozoospermic, 9 ASA positive, 6 dyspermic, 5 with genital tract inflammation, 5 azoospermic, 3 with genital tract obstruction—and demonstrated the presence of sFasL using Western blotting. However, there was no apparent relationship between presence of FasL and ASA presence. A much larger number of patients would be needed to correlate sFasL with antisperm autoimmunization.p

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Authors and Affiliations

  1. Deptt. of Medical Pathophysiology, Laboratory of Seminology and Immunology of Reproduction, Italy

    Franco Dondero, Loredana Gandini, Francesco Lombardo, Antonio Filippini, Paola Lauretti, Elio Ziparo & Andrea Lenzi

  2. Deptt. of Histology and Medical Embriology, University of Rome, La Sapienza, Rome, Italy

    Antonio Filippini, Paola Lauretti & Elio Ziparo

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  1. Franco Dondero
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  2. Loredana Gandini
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  3. Francesco Lombardo
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  4. Antonio Filippini
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  5. Paola Lauretti
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  6. Elio Ziparo
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  7. Andrea Lenzi
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  1. Gamete Antigen Laboratory, National Institute of Immunology, New Delhi, India

    Satish K. Gupta (Chief) (Chief)

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Dondero, F. et al. (1999). Pathogenetical and Clinical Aspects of Antisperm Immunity. In: Gupta, S.K. (eds) Reproductive Immunology. Springer, Dordrecht. https://doi.org/10.1007/978-94-011-4197-0_24

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  • DOI: https://doi.org/10.1007/978-94-011-4197-0_24

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