Seminal 'priming' for protection from pre-eclampsia - A unifying hypothesis

Sarah A. Robertson, John J. Bromfield, Kelton P. Tremellen

Research output: Contribution to journalArticlepeer-review

101 Citations (Scopus)


Conventional belief holds that an immune response to ejaculate antigens should interfere with fertilisation and establishment of pregnancy. However, emerging evidence now supports the opposing view - that insemination acts to activate maternal immune mechanisms exerting a positive effect on reproductive events. In a response well documented in rodents, semen triggers an influx of antigen-presenting cells into the female reproductive tract which process and present paternal ejaculate antigens to elicit activation of lymphocytes in the adaptive immune compartment. Transforming growth factor beta (TGFβ), a cytokine present in abundance in seminal plasma, initiates this inflammatory response by stimulating the synthesis of pro-inflammatory cytokines and chemokines in uterine tissues. Lymphocyte activation is evident in lymph nodes draining the uterus and leads to hypo-responsiveness in T-cells reactive with paternal alloantigens. TGFβ has potent immune-deviating effects and is likely to be the key agent in skewing the immune response against a Type-1 bias. Prior exposure to semen in the context of TGFβ can be shown to be associated with enhanced fetal-placental development late in gestation. In this paper, we review the experimental basis for these claims and propose the hypothesis that, in women, the partner-specific protective effect of insemination in pre-eclampsia might be explained by induction of immunological hypo-responsiveness conferring tolerance to histocompatibility antigens present in the ejaculate and shared by the conceptus.

Original languageEnglish
Pages (from-to)253-265
Number of pages13
Issue number2
Publication statusPublished - Aug 2003
Externally publishedYes


  • Leukocytes
  • Pre-eclampsia
  • Semen
  • Seminal plasma
  • Transforming growth factor-β


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