Immune cell activation by trophoblast-derived microvesicles is mediated by syncytin 1
Article first published online: 23 APR 2012
© 2012 The Authors. Immunology © 2012 Blackwell Publishing Ltd
Volume 136, Issue 2, pages 184–191, June 2012
How to Cite
Holder, B. S., Tower, C. L., Forbes, K., Mulla, M. J., Aplin, J. D. and Abrahams, V. M. (2012), Immune cell activation by trophoblast-derived microvesicles is mediated by syncytin 1. Immunology, 136: 184–191. doi: 10.1111/j.1365-2567.2012.03568.x
- Issue published online: 23 APR 2012
- Article first published online: 23 APR 2012
- Accepted manuscript online: 20 FEB 2012 02:02PM EST
- Received 11 November 2011; revised 18 January 2012; accepted 30 January 2012.
- human endogenous retrovirus;
- immune cells;
Envelope glycoproteins of human endogenous retrovirus (HERV), such as syncytin 1 (HERV-W), are highly expressed in the placenta and some family members have immunomodulatory properties. Placental microvesicles (MV), which are shed into the maternal circulation during pregnancy, have been demonstrated to induce immune cell activation. Therefore, the aim of this study was to investigate the immunological properties of the highly expressed placental HERV-W protein, syncytin 1, and its potential involvement in placental MV modulation of immune cell activity. The MV shed from first trimester, normal term and pre-eclamptic term placentas, and from the BeWo trophoblast cell line, all contain syncytin 1. Recombinant syncytin 1 and syncytin 1-positive BeWo trophoblast MV both induced peripheral blood mononuclear cell (PBMC) activation, indicated through production of cytokines and chemokines. Reducing syncytin 1 content in BeWo MV inhibited PBMC activation. Recombinant syncytin 1 and syncytin-1-positive BeWo MV dampened PBMC responses to lipopolysaccharide challenge. Our findings suggest that syncytin 1 is shed from the placenta into the maternal circulation in association with MV, and modulates immune cell activation and the responses of immune cells to subsequent lipopolysaccharide stimulation. These studies implicate placental MV-associated HERV in fetal regulation of the maternal immune system.