Recurrent miscarriages: What is the role of cytokines?

Calleja‐Agius, Jean; Brincat, Mark

doi:10.1080/09513590802288275

Cited by 23 publications

(14 citation statements)

References 52 publications

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“…In patients suffering from implantation failure and recurrent pregnancy loss, the production of Th1 cytokines from isolated T-cells is increased relative to patients with normal pregnancies [44,45], our data from the CBA/CaH x DBA/2J confirms this. In addition, in the third trimester of pregnancy T-cells from patients with pregnancies complicated with IUGR express greater levels of IFN γ than those from normal pregnant controls [7].…”

Section: Discussionsupporting

confidence: 77%

NF-kB Regulation in T-cells in Pregnancy is Mediated via Fas/FasL Interactions: The Signal for which is Derived from Exosomes Present in Maternal Plasma

McCracken¹,

Hadfield²,

Yenson³

et al. 2016

Reproductive Immunol Open Acc

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Background: Regulated suppression of maternal Th1 immunity is necessary for normal pregnancy since inappropriate Th1 responses results in increased pregnancy loss and complications including intrauterine growth restriction (IUGR). We have shown that suppression of the p65 subunit of NF-κB in maternal T-cells underlies this change in T-cell responses. This study aimed to determine mechanism(s) that control p65 suppression.

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Section: Discussionsupporting

confidence: 77%

NF-kB Regulation in T-cells in Pregnancy is Mediated via Fas/FasL Interactions: The Signal for which is Derived from Exosomes Present in Maternal Plasma

McCracken¹,

Hadfield²,

Yenson³

et al. 2016

Reproductive Immunol Open Acc

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“…The scenario can be compared with HIV-infected children who have increased production of IgG, IgA, and IgE that do not confer protection against HIV, in presence of

T-cell depletion ( Shearer et al 2000 ). During healthy pregnancy, the immune system changes towards higher Th2 cytokine levels ( Calleja-Agius and Brincat 2008 ) and, as a result, the child is born with Th2 dominated immune response. After birth, the immune system requires maturation of the Th1 cytokine response to achieve effective host resistance to infections ( Dietert and Zelikoff 2008 ).…”

Section: Discussionmentioning

confidence: 99%

Humoral Immunity in Arsenic-Exposed Children in Rural Bangladesh: Total Immunoglobulins and Vaccine-Specific Antibodies

Raqib

Ahmed

Ahsan

et al. 2017

Environ Health Perspect

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Background:Early-life arsenic exposure has been associated with reduced cell-mediated immunity, but little is known about its effects on humoral immunity.Objective:We evaluated whether prenatal and childhood arsenic exposure was associated with humoral immune function in school-aged children.Methods:Children born in a prospective mother–child cohort in rural Bangladesh were immunized with measles, mumps, and rubella (MMR) vaccines at 9 years of age (n=525). Arsenic exposure was assessed in urine (U-As), from mothers during pregnancy and their children at 4.5 and 9 years of age. Total IgG (tIgG), tIgE, tIgA, and MMR-specific IgG concentrations were measured in plasma using immunoassays.Results:Arsenic exposure was positively associated with child tIgG and tIgE, but not tIgA. The association with tIgG was mainly apparent in boys (p for interaction=0.055), in whom each doubling of maternal U-As was related to an increase in tIgG by 28mg/dL. The associations of U-As at 9 years with tIgG and tIgE were evident in underweight children (p for interaction <0.032). Childhood arsenic exposure tended to impair mumps-specific vaccine response, although the evaluation was complicated by high preimmunization titers. Postimmunization mumps–specific IgG titers tended to decrease with increasing U-As at 4.5 and 9 years of age [regression coefficient (normalβ)=−0.16; 95% confidence interval (CI): −0.33, 0.01; p=0.064 and β=−0.12; 95% CI: −0.27, −0.029; p=0.113, respectively) in 25% children with the lowest preexisting mumps-specific IgG titers.Conclusions:Arsenic exposure increased tIgG and tIgE in plasma, and tended to decrease mumps-specific IgG in children at 9 years of age. https://doi.org/10.1289/EHP318

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“…Tumor necrosis factor α menyebabkan nekrosis pada janin dan meningkatkan resiko terjadinya kontraksi rahim sehingga mengakibatkan janin mengalami aborsi [3]. Selain itu IFN-γ dapat menginduksi dan mengaktifkan sel natural killer yang ditemukan pada darah perifer perempuan yang mengalami aborsi [44].…”

Section: Pengaruh Infeksi Malaria Pada Janinunclassified

Malaria Pada Kehamilan Dan Konsekuensinya Pada Ibu Dan Janin

Rahmah

2017

JIM

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ABSTRAKMalaria merupakan penyakit infeksi yang masih menjadi masalah kesehatan utama di dunia. Malaria menyerang individu tampa membedakan umur dan jenis kelamin tidak terkecuali ibu hamil. Ibu hamil memiliki resiko terserang malaria oleh parasit Plasmodium lebih berat di bandingkan dengan wanita tidak hamil. Ketika seorang hamil akan terjadi supresi imun baik humoral maupun seluler Tujuan makalah ini untuk membahas mekanisme terjadinya malaria pada kehamilan dan konsekuensinya pada ibu dan janin. Adhesi parasit dengan reseptor Chondroitin Sulfate A (CSA) dan Hyaluronic Acid (HA) di plasenta dapat memicu proses inflamasi yang melibatkan sekresi sitokin. Komponen inflamasi yang muncul setelah akumulasi parasit di plasenta berasosiasi dengan patologi imun pada Pregnancy-Associated Malaria (PAM), seperti penebalan membran sitotrofoblas yang mengganggu aliran darah, menghambat transfer IgG melintasi plasenta dan pertukaran nutrisi dari ibu ke janin sehingga terjadi lesi pada plasenta. Selama kehamilan yang terinfeksi malaria terjadi proses cytoadherence di mediasi oleh protein Plasmodium falciparum Erythrocyte Membran Protein-1 (PfEMP-1) dikode oleh gen Var2 CSA yang mengikat reseptor di plasenta hal ini menyebabkan sekuestrasi eritrosit terinfeksi di sel endotel yang mengakibatkan terjadinya anemia pada ibu sedangkan pada janin menyebabkan berat badan lahir rendah, lahir prematur dan lahir mati. Kata kunci : Malaria, Ibu Hamil, Janin ABSTRACTMalaria is an infectious disease remains a major health problem in the world. Malaria attacks without differentiating individual age and sex of pregnant women are no exception. Pregnant women have a risk of malaria by Plasmodium parasites is more severe in comparison with non-pregnant women. When a pregnancy will occur immunosuppression both humoral and cellular purpose of this paper is to discuss the mechanism of occurrence of malaria in pregnancy and its consequences on the mother and fetus. Parasite adhesion receptors Chondroitin Sulfate A (CSA) and Hyaluronic Acid (HA) in the placenta can trigger an inflammatory process involving the secretion of cytokines. Inflammatory component that appears after the accumulation of parasites in the placenta is associated with immune pathology in the Pregnancy-Associated Malaria (PAM), such as thickening of the membrane cytotrophoblasts that disrupt blood flow, inhibiting the transfer of IgG across the placenta and the exchange of nutrients from mother to fetus, causing lesions in the placenta. Malaria infection during pregnancy is a process of mediation by protein cytoadherence in Plasmodium falciparum erythrocyte membrane protein-1 (PfEMP-1) encoded by genes that bind to receptors on Var2CSA this causes placental sequestration of infected erythrocytes on endothelial cells resulting in anemia in pregnant while on fetus causes low birth weight, premature birth and stillbirth.

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Recurrent miscarriages: What is the role of cytokines?

Cited by 23 publications

References 52 publications

NF-kB Regulation in T-cells in Pregnancy is Mediated via Fas/FasL Interactions: The Signal for which is Derived from Exosomes Present in Maternal Plasma

NF-kB Regulation in T-cells in Pregnancy is Mediated via Fas/FasL Interactions: The Signal for which is Derived from Exosomes Present in Maternal Plasma

Humoral Immunity in Arsenic-Exposed Children in Rural Bangladesh: Total Immunoglobulins and Vaccine-Specific Antibodies

Malaria Pada Kehamilan Dan Konsekuensinya Pada Ibu Dan Janin

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