Skip to main page content
U.S. flag

An official website of the United States government

Dot gov

The .gov means it’s official.
Federal government websites often end in .gov or .mil. Before sharing sensitive information, make sure you’re on a federal government site.

Https

The site is secure.
The https:// ensures that you are connecting to the official website and that any information you provide is encrypted and transmitted securely.

Access keys NCBI Homepage MyNCBI Homepage Main Content Main Navigation
Editorial
. 2012 Nov;60(5):1114-6.
doi: 10.1161/HYPERTENSIONAHA.112.202747. Epub 2012 Sep 24.

Complement activation in pregnancy: too much of a good thing?

Editorial

Complement activation in pregnancy: too much of a good thing?

Jeffrey S Gilbert et al. Hypertension. 2012 Nov.
No abstract available

PubMed Disclaimer

Figures

Figure 1
Figure 1
Simplistic schematic of complement system activation depicting regulators and complement components measured by Buurma and others. The complement system is activated via three pathways: Classical, lectin and alternative. All three pathways result in formation of C3 convertase to cleave C3 into a covalently bound C3b fragment and a fluid phase C3a fragment. C1q is indicative of classical pathway involvement, and mannose binding lectin (MBL) indicates lectin pathway involvement. With activation of either the classical or lectin pathway, C4b covalently binds locally to invader or self surfaces. C4b either participates in formation of C3 convertase, or is degraded to bound C4d. With alternative pathway activation, Factor B is cleaved to form Bb which participates in formation of the alternative pathway C3 convertase. Properdin stabilizes C3 convertase formed with alternative pathway activation. C3b can either participate as part of the C5 convertase complex to cleave C5 or be degraded to bound C3d. C5b, C6, C7, C8 and C9 assemble in cell membranes to form membrane attack complex (MAC) which deteriorates membrane potential and induces cell lysis. Regulators present on the trophoblast membrane as well as numerous cells in mother and fetus include MCP (CD46), DAF (CD55), and CD59. MCP, or membrane cofactor protein, facilitates degradation of C3b and C4b so they do not continue as part of the C3 convertase. DAF, or decay-accelerating factor, facilitates decay of convertases assembled from activation of any of the pathways, and CD59 hampers assembly of MAC.

Comment on

References

    1. Steegers EA, von Dadelszen P, Duvekot JJ, Pijnenborg R. Pre-eclampsia. The Lancet. 2010;376:631–644. - PubMed
    1. Buurma A, Cohen D, Veraar K, Schonkeren D, Claas FHJ, Bruijin J, Bloemenkamp K, Baelde H. Preeclampsia Is Characterized By Placental Complement Dysregulation. Hypertension. 2012;xx:xxx. - PubMed
    1. Tedesco F, Radillo O, Candussi G, Nazzaro A, Mollnes TE, Pecorari D. Immunohistochemical detection of terminal complement complex and S protein in normal and pre-eclamptic placentae. Clin Exp Immunol. 1990;80:236–240. - PMC - PubMed
    1. Derzsy Z, Prohaszka Z, Rigo J, Jr, Fust G, Molvarec A. Activation of the complement system in normal pregnancy and preeclampsia. Mol Immunol. 2010;47:1500–1506. - PubMed
    1. Sinha D, Wells M, Faulk WP. Immunological studies of human placentae: complement components in pre-eclamptic chorionic villi. Clin Exp Immunol. 1984;56:175–184. - PMC - PubMed

Substances