Autoimmunity and Recurrent Pregnancy Losses

Cervera, Ricard; Balasch, Juan

doi:10.1007/s12016-009-8179-1

Cited by 25 publications

(11 citation statements)

References 65 publications

(49 reference statements)

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“…The reason for this remains unclear, but aPL have been linked to a wide range of factors involved in successful pregnancy. Several pro-thrombotic mechanisms have been proposed including alterations in eicosanoid balance, cross reactivity with glycosaminoglycans and interference with the function of natural inhibitors of coagulation such as annexin V present on the surface of the syncytiotrophoblasts (Cervera & Balasch 2009). aPL have also been shown to have direct placental effects and are capable of inhibiting both trophoblast differentiation and invasion, and may also affect endometrial decidualisation to an extent that may be sufficient to cause the loss of a pregnancy that is compromised by other factors (Buckingham & Chamley 2009).…”

Section: Recurrent Miscarriagementioning

confidence: 99%

Remodelling at the maternal–fetal interface: relevance to human pregnancy disorders

Cartwright¹,

Fraser²,

Leslie³

et al. 2010

Reproduction

238

144

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In human pregnancy, successful placentation and remodelling of the uterine vasculature require the integration of a number of stages, which are crucial for a healthy pregnancy. As the demands of the developing fetus for nutrients and oxygen increase, the capacity of the maternal blood vessels to supply this must be altered radically, with deficiencies in this process implicated in a number of dangerous pregnancy complications. The complex signalling networks that regulate these tightly co-ordinated events are becoming clearer as more studies of early pregnancy are performed. It is the aim of this review to draw together our knowledge of events that occur to facilitate a successful pregnancy ranging from the preparation for implantation, through the invasion and differentiation of the trophoblast and the regulation of these processes by other cells within the decidual environment, to the active role that the trophoblast and maternal immune cells play in facilitating the remodelling of the uterine spiral arteries. The events involved in a healthy pregnancy will then be compared to aberrant placentation and remodelling, which are characteristics of many pregnancy disorders, and recent advances in detection of abnormal placental development will also be discussed.

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Section: Recurrent Miscarriagementioning

confidence: 99%

Remodelling at the maternal–fetal interface: relevance to human pregnancy disorders

Cartwright¹,

Fraser²,

Leslie³

et al. 2010

Reproduction

238

144

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“…An assortment of hormones, cytokines, and immunoregulatory cells within the environment works to suppress the immune response that would normally react to the foreign entities of the fetus, while altering and recruiting immune populations that support embryo implantation and growth [2]. A disruption in the modulation of the maternal immune response can prove to be detrimental to the survival and growth of the fetus, whereby uncontrolled inflammation and chronic autoimmune syndromes can result in miscarriage [3][4][5]. Recurrent miscarriage, defined as three miscarriages or more, presents a significant barrier for child-bearing and affects 1-4% of the population [1,6].…”

Section: Introductionmentioning

confidence: 99%

Interleukin-15 is required for maximal lipopolysaccharide-induced abortion

Lee

Kandiah

Karimi

et al. 2013

Journal of Leukocyte Biology

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The maternal immune response during pregnancy is critical for the survival of the fetus yet can be detrimental during infection and inflammation. Previously, IL-15 has been observed to mediate inflammation during LPS-induced sepsis. Therefore, we sought to determine whether IL-15 mediates the inflammatory process during LPS-induced abortion through the use of IL-15(-/-) and WT mice. Administration of 2.5 μg LPS i.p. on gd 7.5 drastically reduced fetal viability in WT mice, whereas it had a minimal effect on fetal survival in IL-15(-/-) mice. The uteroplacental sites of LPS-treated WT mice were characterized by vast structural degradation and inflammation compared with treated IL-15(-/-) and untreated controls. This suggests that IL-15 may mediate the inflammation responsible for LPS-induced resorption. As IL-15(-/-) mice are deficient in NK cells and resistant to LPS-induced abortion, these effects suggest that IL-15 may mediate abortion through their homeostatic and/or activation effects on NK cells. WT uteroplacental units exposed to LPS had an increase in the overall number and effector number of NK cells compared with their control counterparts. Furthermore, NK cell depletion before administration of LPS in WT mice partially restored fetal viability. Overall, this paper suggests that IL-15 mediates the inflammatory environment during LPS-induced fetal resorption, primarily through its effects on NK cells.

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“…Regarding our patient it is unclear whether these antibodies alone were directly pathogenic and caused maternal vascular malperfusion on placenta or they were “only” a persistent marker of an underlying SLE placenta damage. In particular, such patients with SLE and/or APS are at high risk for placental insufficiency and intrauterine growth restriction as a result of inflammation rather than thrombosis at the maternal-fetal interface [23]. In our case, it is perhaps more likely that the placental dysfunction has led to a premature rupture of membranes and the later developed acute chorioamnionitis is a second finding in this context.…”

Section: Discussionmentioning

confidence: 73%

Live birth pregnancy outcome after first in vitro fertilization treatment in a patient with Systemic Lupus Erythematosus and isolated high positive IgA anti-β2glycoprotein I antibodies: a case report

2017

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AbstractIgA anti-β2glycoprotein I antibodies (IgA-anti-β2GPI) seems to be the most prevalent isotype in patients with Systemic Lupus Erythematosus (SLE) with a significant association to thrombotic events. Both SLE and antiphospholipid syndrome (APS) can be associated with implantation failure, fetal loss and obstetric complications. Recent reports highlight the clinical value of IgA-anti-β2GPI determination in supporting in vitro fertilization (IVF) treatment and IVF pregnancy outcomes. We report a 36-year-old female diagnosed with SLE, endometriosis and unexplained infertility. Conventional APS markers were consistently negative: anti-cardiolipin (aCL) and anti-β2GPI: IgG/IgM. She was then tested with reports of repeatedly high IgA-anti-β2GPI and tested positive from 2014 after IgA (aCL; anti-β2GPI) were established in our APS diagnostic panel. She underwent successful first IVF procedure with a 30 week live birth pregnancy outcome. During the follow up no lupus flare, thrombosis or ovarian hyperstimulation syndrome were registered. Serum IgA anti-β2GPI and anti-dsDNA levels declined statistically significant during the second and third trimester. Titres of IgA-anti-β2GPI remained lower postpartum as well. This case highlights the clinical importance of IgA-anti-β2GPI testing for family planning, assisted reproduction and pregnancy in women with SLE and/or APS.

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Autoimmunity and Recurrent Pregnancy Losses

Cited by 25 publications

References 65 publications

Remodelling at the maternal–fetal interface: relevance to human pregnancy disorders

Remodelling at the maternal–fetal interface: relevance to human pregnancy disorders

Interleukin-15 is required for maximal lipopolysaccharide-induced abortion

Live birth pregnancy outcome after first in vitro fertilization treatment in a patient with Systemic Lupus Erythematosus and isolated high positive IgA anti-β2glycoprotein I antibodies: a case report

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