The complement system in the pathophysiology of pregnancy

Mol Immunol. 2006 Jan;43(1-2):68-77. doi: 10.1016/j.molimm.2005.06.017.


A fully active complement system deriving from the maternal circulation as well as from local production by various cell source is present in the placenta. The role of this system at the placental level, as in any other tissue in the body, is to protect both the fetus and the mother against infectious and other toxic agents. As fetal tissues are semi-allogeneic and alloantibodies commonly develop in the mother, the placenta is potentially subject to complement-mediated immune attack at the feto-maternal interface with the potential risk of fetal loss. Uncontrolled complement activation is prevented in successful pregnancy by the three regulatory proteins DAF, MCP and CD59 positioned on the surface of trophoblasts. The critical role played by these complement regulators is supported by the embryonic lethality observed in mice deficient in the complement regulator Crry. Excessive complement activation in the placenta places the fetus at risk for growth restriction or death. The role played by the complement system in the fetal damage induced by anti-phospholipid antibodies in a mouse model will be examined.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Antibodies, Antiphospholipid / immunology
  • Complement Activating Enzymes / genetics
  • Complement Activating Enzymes / immunology
  • Complement Activation / genetics
  • Complement Activation / immunology*
  • Complement Inactivator Proteins / genetics
  • Complement Inactivator Proteins / immunology*
  • Female
  • Fetal Death / genetics
  • Fetal Death / immunology
  • Fetal Death / pathology
  • Fetomaternal Transfusion / genetics
  • Fetomaternal Transfusion / immunology*
  • Fetomaternal Transfusion / pathology
  • Humans
  • Isoantibodies / immunology*
  • Maternal-Fetal Exchange / genetics
  • Maternal-Fetal Exchange / immunology*
  • Mice
  • Mice, Knockout
  • Pregnancy
  • Receptors, Complement / deficiency
  • Receptors, Complement / immunology
  • Receptors, Complement 3b
  • Trophoblasts / immunology*
  • Trophoblasts / pathology


  • Antibodies, Antiphospholipid
  • Complement Inactivator Proteins
  • Cr1l protein, mouse
  • Isoantibodies
  • Receptors, Complement
  • Receptors, Complement 3b
  • Complement Activating Enzymes