The complement system and adverse pregnancy outcomes.
The complement system and adverse pregnancy outcomes.
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DOI：
10.1016/j.molimm.2015.02.030
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发表时间：
2015-09
影响因子：
3.6
通讯作者：
Burwick RM
中科院分区：
文献类型：
--
作者：
Regal JF;Gilbert JS;Burwick RM
Adverse pregnancy outcomes significantly contribute to morbidity and mortality for mother and child, with lifelong health consequences for both. The innate and adaptive immune system must be regulated to insure survival of the feta allograft, and the complement system is no exception. An intact complement system optimizes placental development and function and is essential to maintain host defense and fetal survival. Complement regulation is apparent at the placental interface from early pregnancy with some degree of complement activation occurring normally throughout gestation. However, a number of pregnancy complications including early pregnancy loss, fetal growth restriction, hypertensive disorders of pregnancy and preterm birth are associated with excessive or misdirected complement activation, and are more frequent in women with inherited or acquired complement system disorders or complement gene mutations. Clinical studies employing complement biomarkers in plasma and urine implicate dysregulated complement activation in components of each of the adverse pregnancy outcomes. In addition, mechanistic studies in rat and mouse models of adverse pregnancy outcomes address the complement pathways or activation products of importance and allow critical analysis of the pathophysiology. Targeted complement therapeutics are already in use to control adverse pregnancy outcomes in select situations. A clearer understanding of the role of the complement system in both normal pregnancy and complicated or failed pregnancy will allow a rational approach to future therapeutic strategies for manipulating complement with the goal of mitigating adverse pregnancy outcomes, preserving host defense, and improving long term outcomes for both mother and child.
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DOI：
10.4049/jimmunol.0903678
发表时间：
2010-11-01
期刊：
Journal of immunology (Baltimore, Md. : 1950)
影响因子：
--
作者：
Amara U;Flierl MA;Rittirsch D;Klos A;Chen H;Acker B;Brückner UB;Nilsson B;Gebhard F;Lambris JD;Huber-Lang M
通讯作者：
Huber-Lang M
DOI：
10.1136/bmj.f6564
发表时间：
2013-11-07
期刊：
BMJ (Clinical research ed.)
影响因子：
--
作者：
Ananth CV;Keyes KM;Wapner RJ
通讯作者：
Wapner RJ
影响因子：
2.6
作者：
Baj-Krzyworzeka, M;Majka, M;Ratajczak, MZ
通讯作者：
Ratajczak, MZ
影响因子：
8.3
作者：
Burwick, Richard M.;Easter, Sarah Rae;Feinberg, Bruce B.
通讯作者：
Feinberg, Bruce B.
影响因子：
2.6
作者：
Aggarwal R;Sestak AL;D'Souza A;Dillon SP;Namjou B;Scofield RH
通讯作者：
Scofield RH