The role of complement in pregnancy and fetal loss.
In the United States, between 1 and 3% of women suffer recurrent miscarriages; 50-70% of all conceptions fail. Although in the majority of affected women the cause of recurrent miscarriages is unknown, an immune mechanism involving the inappropriate and subsequently injurious recognition of the conceptus by the mother's immune system has been proposed. Murine models have recently been developed that are relevant to this issue. We and others have identified a novel role for complement as an early effector in the pathway leading to pregnancy loss associated with placental inflammation. Indeed, it appears that inhibition of complement activation is an absolute requirement for normal pregnancy, and that in the antiphosphospholid syndrome overwhelming activation of complement triggered by antibodies (Ab) deposited in placenta leads to fetal injury. Identification of complement activation as a mediator of pregnancy loss and definition of the complement components necessary to trigger such injury is likely to lead to a better understanding of its pathogenesis and to new and improved treatments.
Girardi
Guillermina
G
Department of Medicine, Hospital for Special Surgery, Weill Medical College of Cornell University, 535 East 70th Street, New York, NY 10021, USA.
Salmon
Jane B
JB
D037881:Aborted Fetus / Q000276:immunology*; D000022:Abortion, Spontaneous / Q000276:immunology*; D000818:Animals; D017152:Antibodies, Antiphospholipid / Q000276:immunology; D003167:Complement Activation; D050577:Complement C3-C5 Convertases / Q000378:metabolism; D005260:Female; D006084:Graft Rejection; D006801:Humans; D007108:Immune Tolerance; D051379:Mice; D008807:Mice, Inbred BALB C; D011247:Pregnancy
D017152:Antibodies, Antiphospholipid; D050577:Complement C3-C5 Convertases