The complement system at the feto-maternal interface: friend or foe?
Article first published online: 16 AUG 2002
American Journal of Reproductive Immunology
Volume 48, Issue 3, pages 142–143, September 2002
How to Cite
Tedesco, F., Bulla, R., Bossi, F., Macor, Paolo., Radillo, O. and De Seta, F. (2002), The complement system at the feto-maternal interface: friend or foe?. American Journal of Reproductive Immunology, 48: 142–143. doi: 10.1034/j.1600-0897.2002.00025.x
- Issue published online: 16 AUG 2002
- Article first published online: 16 AUG 2002
- Cited By
The complement system is an essential component of the innate immune system and functions as a double-edged weapon providing on the one hand an effective means of defence and yet causing cell and tissue damage. The liver represents the major source of complement components present in the blood that circulates in decidua and in intervillous space. We have examined macrophages, endothelial and stromal cells and trophoblast as the most likely candidates for local production of complement components. All these cells produce primarily C4 and C3 and various other components under the control of locally available cytokines. We have recently examined the distribution and the role of C1q and of the related proteins, MBL and emilin, a component of the elastic fibers. While emilin is evenly distributed in the decidual stroma, both C1q and MBL appear to be present preferentially on the wall of blood vessels. The results of in vitro experiments have shown that extravillous trophoblast use C1q and emilin to adhere and to migrate in decidua. Deposits of complement components are seen particularly on the wall of spiral arteries. C1q can be detected on the endothelium and also in the subendothelium, where we detect deposition also of the terminal complex. Placental cells are protected from the undesired effect of complement activation products by acquiring complement regulators from the fluid phase or by expressing regulators on the cell surface including DAF, MCP and CD59.