Complement component deposition in utero-placental (spiral) arteries in normal human pregnancy

Wells, Michael; Bennett, JA; Bulmer, Judith N.; Jackson, Peter A.; Holgate, C S

doi:10.1016/0165-0378(87)90040-4

Cited by 47 publications

(23 citation statements)

References 13 publications

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“…[36,37] 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 maternal -fetal interface. [36] Though activated complement components are present in normal placentas, [38,39] it appears that uncontrolled complement activation is prevented in successful pregnancy by three regulatory proteins present on the trophoblast membrane. [40,41] Two of these membrane-bound proteins, DAF and MCP, regulate the activation of C3 and C4 on the surface of cells.…”

Section: Fetal Tolerance and Complementmentioning

confidence: 98%

The Role of Complement in Pregnancy and Fetal Loss

Girardi

Salmon

2003

Autoimmunity

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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.

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Section: Fetal Tolerance and Complementmentioning

confidence: 98%

The Role of Complement in Pregnancy and Fetal Loss

Girardi

Salmon

2003

Autoimmunity

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“…Its success is dependent upon some degree of uterine inflammation, as has been shown by several studies in human beings and in animals [4 -6]. The importance of the immune system in placentation is further underscored by the detection of inflammatory cells [7] and mediators, such as cytokines [8,9] and components of the complement system [10] in placentas of normal uncomplicated pregnancies. Because of the local presence of complement regulators, deposition of complement in the placenta usually does not lead to tissue damage [11].…”

Section: Introductionmentioning

confidence: 95%

Mannose-binding lectin genotypes and pre-eclampsia: A case-control study

et al. 2007

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“…There is conflicting evidence on the deposition of C components in decidual vessels in normal and pathologic pregnancies (Hustin et al, 1983;Kitzmiller et al, 1981;Wells et al, 1987). We have re-examined this issue looking in particular at the presence of C components on DECs in view of the special interaction of these cells with endovascular trophoblast resulting in their partial replacement.…”

Section: C1q Is Localized On Decsmentioning

confidence: 99%

Decidual endothelial cells express surface-bound C1q as a molecular bridge between endovascular trophoblast and decidual endothelium

Bulla

Agostinis

Bossi

et al. 2008

Molecular Immunology

113

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This study was prompted by the observation that decidual endothelial cells (DECs), unlike endothelial cells (ECs) of blood vessels in normal skin, kidney glomeruli and brain, express surface-bound C1q in physiologic pregnancy. This finding was unexpected, because deposits of C1q are usually observed in pathologic conditions and are associated with complement activation. In the case of DECs, we failed to detect immunoglobulins and C4 co-localized with C1q on the cell surface. Surprisingly, DECs expressed mRNA for the three chains of C1q and secreted detectable level of this component in serum-free medium. The ability to synthesize C1q is acquired by DECs during pregnancy and is not shared by ECs obtained from endometrium and from other sources. Cell-associated C1q has a molecular weight similar to that of secreted C1q and is released from DECs following treatment with heparinase or incubation at low pH. This suggests that C1q binds to DECs and it is not constitutively expressed on the cell surface. C1q is localized at contact sites between endovascular trophoblast and DECs and acts as an intercellular molecular bridge because adhesion of endovascular trophoblast to DECs was inhibited by antibodies to C1q and to a receptor recognizing its globular portion expressed on trophoblast.

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Complement component deposition in utero-placental (spiral) arteries in normal human pregnancy

Cited by 47 publications

References 13 publications

The Role of Complement in Pregnancy and Fetal Loss

The Role of Complement in Pregnancy and Fetal Loss

Mannose-binding lectin genotypes and pre-eclampsia: A case-control study

Decidual endothelial cells express surface-bound C1q as a molecular bridge between endovascular trophoblast and decidual endothelium

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