Soluble CD52 mediates immune suppression by human seminal fluid

Front Immunol. 2024 Dec 16:15:1497889. doi: 10.3389/fimmu.2024.1497889. eCollection 2024.

Abstract

Seminal fluid provides for the carriage and nutrition of sperm, but also modulates immunity to prevent allo-rejection of sperm by the female. Immune suppression by seminal fluid has been associated with extracellular vesicles, originally termed prostasomes, which contain CD52, a glycosylated glycophosphoinositol-anchored peptide released from testicular epithelial cells. Previously, we reported that human T cell-derived CD52, bound to the danger-associated molecular pattern protein, high mobility group box 1 (HMGB1), suppresses T cell function via the inhibitory sialic acid-binding immunoglobulin-like lectin-10 (Siglec-10) receptor. Here we show that human seminal fluid contains high concentrations of CD52 complexed with HMGB1, which mediates T cell suppression indirectly via Siglec-7 on antigen-presenting cells. Proliferation of natural killer (NK) cells, which express Siglec-7 and play a key role in the immune defence of the uterus, was directly suppressed by seminal fluid CD52. These findings elucidate a critical function of seminal fluid to suppress cellular immunity and facilitate reproduction.

Keywords: CD52; HMGB1; NK cell; Siglec-7; T cell; seminal fluid.

MeSH terms

  • Antigens, Differentiation, Myelomonocytic / immunology
  • Antigens, Differentiation, Myelomonocytic / metabolism
  • CD52 Antigen* / immunology
  • CD52 Antigen* / metabolism
  • Female
  • HMGB1 Protein
  • Humans
  • Immune Tolerance
  • Killer Cells, Natural* / immunology
  • Killer Cells, Natural* / metabolism
  • Lectins / immunology
  • Lectins / metabolism
  • Male
  • Semen* / immunology
  • Semen* / metabolism
  • T-Lymphocytes / immunology
  • T-Lymphocytes / metabolism

Substances

  • CD52 Antigen
  • CD52 protein, human
  • SIGLEC7 protein, human
  • HMGB1 protein, human
  • Antigens, Differentiation, Myelomonocytic
  • Lectins
  • HMGB1 Protein

Grants and funding

The author(s) declare financial support was received for the research, authorship, and/or publication of this article. This work was supported by grants from the Australian National Health and Medical Research Council (NHMRC) to LH (Program Grant 1037321, Project Grant 1051484, Senior Principal Research Fellowship 637301). The work was made possible through Victorian State Government Operational Infrastructure Support and NHMRC Research Institute Infrastructure Support Scheme.