Dysregulated Complement Activation as a Common Pathway of Injury in Preeclampsia and Other Pregnancy Complications

被引:84
|
作者
Lynch, A. M. [2 ]
Salmon, J. E. [1 ]
机构
[1] Hosp Special Surg, Weill Cornell Med Coll, Autoimmun & Inflammat Program, New York, NY 10021 USA
[2] Univ Colorado Denver, Sch Med, Dept Obstet & Gynecol, Aurora, CO 80045 USA
关键词
Complement; Preeclampsia; Inflammation; SYSTEMIC-LUPUS-ERYTHEMATOSUS; HEMOLYTIC-UREMIC SYNDROME; DECAY-ACCELERATING FACTOR; ELEVATED LIVER-ENZYMES; CIRCULATING ANGIOGENIC FACTORS; MEMBRANE COFACTOR PROTEIN; C1S-C1 INHIBITOR COMPLEX; ANTIPHOSPHOLIPID ANTIBODY; HUMAN TROPHOBLAST; REGULATORY PROTEIN;
D O I
10.1016/j.placenta.2010.03.010
中图分类号
Q [生物科学];
学科分类号
07 ; 0710 ; 09 ;
摘要
The complement system protects the host against invading organisms, initiates inflammation and dispose of immune complexes and the products of inflammatory injury. The complement system provides an important link between the innate and adaptive immune systems. Experimental observations suggest that increased complement activation causes and/or perpetuates inflammation during pregnancy. Recent studies suggest a link between complement activation and preeclampsia. Excessive activation or insufficient regulation of complement recruits leukocytes and unleashes potent inflammatory and anti-angiogenic mediators associated with placental insufficiency and maternal endothelial dysfunction characteristic of preeclampsia. We review the animal and human studies that link complement activation and pathogenic events in preeclampsia, present evidence that activation of the complement system is associated with the development of preeclampsia and provides new targets to prevent its complications. (C) 2010 Elsevier Ltd. All rights reserved.
引用
收藏
页码:561 / 567
页数:7
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