Mechanisms of active suppression of the immune response to spermatozoa. Review uri icon

Overview

abstract

  • The production of autoantibodies to spermatozoa in males and isoantibodies in females is inhibited both by the physical isolation of spermatozoa from the systemic immune system and by active immunosuppression mechanisms. Lymphoid cells present in the epithelial lining of the rete testis, epididymis, and vas deferens, as well as the human ejaculate, are predominantly T suppressor/cytotoxic cells. Mononuclear cells derived from semen inhibit the in vitro activation of peripheral blood lymphocytes. Soluble specific T suppressor/cytotoxic cell activators in semen or on the sperm surface may be responsible for the predominance of this T cell subset in the male reproductive tract. The activation of T suppressor/cytotoxic cells following coitus may also limit the immune response to spermatozoa in females. Spermatozoa can also initiate immunosuppression, either by selectively inducing T suppressor cells or through the generation of activated complement components that block antibody production. Antisperm antibodies in sera from females may be associated with either a deficiency in the ability of their T suppressor/cytotoxic cells to be induced by factors in semen or by the occurrence in their husbands' ejaculates of microorganisms, antibodies, or other factors that induce T helper lymphocytes. Activated T cells produce interferon gamma, which induces Ia antigen expression on macrophages and allows the female's T helper cells to recognize processed sperm antigens. Recognition of the role of cell-mediated immune functions in the male and female genital tract identifies possible new target sites for the development of contraceptive agents.

publication date

  • June 1, 1988

Research

keywords

  • Autoantibodies
  • Isoantibodies
  • Spermatozoa

Identity

Scopus Document Identifier

  • 0023683366

Digital Object Identifier (DOI)

  • 10.1111/j.1600-0897.1988.tb00204.x

PubMed ID

  • 2973252

Additional Document Info

volume

  • 17

issue

  • 2