The Change of Membrane Complement Regulatory Protein in Chorion of Early Pregnancy

Nishikori, Kyoko; Noma, Jun; Hirakawa, Syuzo; Amano, Tetsuki; Kudo, T

doi:10.1006/clin.1993.1166

Cited by 21 publications

(12 citation statements)

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“…DAF is a complement-modulating factor that is also expressed in the fetomaternal interface and has been implicated in protection of the fetus from rejection (Rooney and Morgan 1990b). The expression of DAF on human trophoblast membranes may protect them from maternal complement-mediated damage in response to microbial infection (Nishikori et al, 1993;Jensen et al, 1995;Fenichel et al, 1995). Our recent results support the notion that there are inherent differences in immunological responsiveness between individuals and that the vitamin D3 system may be important in sustaining LPS-induced CD55 expression (Izban at al.…”

Section: Complement and Complement Inhibitorssupporting

confidence: 76%

Amniotic Fluid and the Fetal Mucosal Immune System

Nowicki

Goldblum

2015

Mucosal Immunology

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Section: Complement and Complement Inhibitorssupporting

confidence: 76%

Amniotic Fluid and the Fetal Mucosal Immune System

Nowicki

Goldblum

2015

Mucosal Immunology

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“…On the syncytiotrophoblast, the differentiated fused trophoblast that lines the intervillous space, all three membrane bound complement regulators are consistently noted in first, second and third trimester placenta i.e. CD46, CD55 and CD59 (Figure 2B) (Holmes et al, 1992; Holmes et al, 1990; Hsi et al, 1991; Lokki et al, 2014; Nishikori et al, 1993). Using trophoblasts isolated from first through third trimester, Holmes (Holmes et al, 1992; Holmes et al, 1990) noted increased presence of all three regulators in second and third trimester.…”

Section: Complement System and Normal Pregnancymentioning

confidence: 93%

The complement system and adverse pregnancy outcomes

Regal

Gilbert

Burwick

2015

Molecular Immunology

134

115

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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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“…DAF protects our tissues from destruction by autologous complement. DAF is expressed in the fetomaternal interface, presumably to protect the fetus from maternal complement cytotoxicity [21,22]. Hypothetically, even a small local imbalance between these factors leading to even a minor activation of the complement may activate detrimental proinflammatory/prostaglandin cascades [23][24][25][26].…”

Section: Pregnancy and The Immune Systemmentioning

confidence: 99%

Urinary tract infection in pregnant women: Old dogmas and current concepts regarding pathogenesis

Nowicki

2002

Curr Infect Dis Rep

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The dogma is that the higher risk of pyelonephritis in pregnant women is explained entirely by anatomic/obstructive changes. If so, gestational pyelonephritis should be caused by random, nonpathogenic bacteria. Instead, gestational pyelonephritis is associated with a narrow group of genetically related Escherichia coli and virulence factors, implicating a more complex pathophysiology. Current concepts in the pathogenesis of nongestational urinary tract infections propose receptor-mediated ascending infection. A pathogen with capacity to recognize various receptors may use receptors in the lower, rather than upper urinary tract, and ascend even the lumen of renal tubules. The immune system of a pregnant mother is modified to accommodate a semiallogeneic fetus. Gestational physiologic/immune adaptations may become additional risk factors, increasing sensitivity to urogenital infection. One could argue that it is not primarily the so-called "obstruction," but rather specific changes in the immune system and host receptors that act in concert with--or become exploited by--bacterial virulence that allow for infection in pregnancy to occur.

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The Change of Membrane Complement Regulatory Protein in Chorion of Early Pregnancy

Cited by 21 publications

References 0 publications

Amniotic Fluid and the Fetal Mucosal Immune System

Amniotic Fluid and the Fetal Mucosal Immune System

The complement system and adverse pregnancy outcomes

Urinary tract infection in pregnant women: Old dogmas and current concepts regarding pathogenesis

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