Placental Villous Expression of <scp>TNF</scp>α and <scp>IL</scp>‐10 and Effect of Oxygen Tension in Euploid Early Pregnancy Failure

Calleja‐Agius, Jean; Jauniaux, Eric; Muttukrishna, Shanthi

doi:10.1111/j.1600-0897.2012.01104.x

Cited by 15 publications

(19 citation statements)

References 58 publications

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“…TNF-α has been shown to be increased in euploid compared to aneuploid miscarriages, as well as increased compared to the euploid pregnancies that survive [13,[72][73][74]79]. This increase has also been noted in their peripheral blood.…”

Section: Tnf-αmentioning

confidence: 68%

“…These cells also release IFN-γ to promote inflammation. It has been shown to be elevated in RPL patients [13,72,78,79,124]. Significant associations between RPL and the IFN-γ(+874) polymorphisms have been found [115,119,120].…”

Section: Ifn-γmentioning

confidence: 95%

“…IL-10 inhibits macrophages and Th1 cell proliferation [76,77]. Th1 cells both produce and are promoted by IFN-γ [11,72,73,78,79]. They secrete IL-12 as well [41].…”

Section: T-helper Lymphocyte-2 Cellsmentioning

confidence: 99%

“…There they express IL-10, TGFβ, and TNFα [10]. TNF-α is produced by all CD4+ T cells [11,[72][73][74][75]. IL-10 inhibits macrophages and Th1 cell proliferation [76,77].…”

Section: T-helper Lymphocyte-2 Cellsmentioning

confidence: 99%

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Immunogenetic contributions to recurrent pregnancy loss

Grimstad

Krieg

2016

J Assist Reprod Genet

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While sporadic pregnancy loss is common, occurring in 15 % of pregnancies, recurrent pregnancy loss (RPL) impacts approximately 5 % of couples. Though multiple causes are known (including structural, hormonal, infectious, autoimmune, and thrombophilic causes), after evaluation, roughly half of all cases remain unexplained. The idiopathic RPL cases pose a challenging therapeutic dilemma in addition to incurring much physical and emotional morbidity. Immunogenetic causes have been postulated to contribute to these cases of RPL. Natural Killer cell, T cell expression pattern changes in the endometrium have both been shown in patients with RPL. Human leukocyte antigen (HLA) and cytokine allelic variations have also been studied as etiologies for RPL. Some of the results have been promising, however the studies are small and have not yet put forth outcomes that would change our current diagnosis and management of RPL. Larger database studies are needed with stricter control criteria before reasonable conclusions can be drawn.

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Section: Tnf-αmentioning

confidence: 68%

Section: Ifn-γmentioning

confidence: 95%

“…IL-10 inhibits macrophages and Th1 cell proliferation [76,77]. Th1 cells both produce and are promoted by IFN-γ [11,72,73,78,79]. They secrete IL-12 as well [41].…”

Section: T-helper Lymphocyte-2 Cellsmentioning

confidence: 99%

“…There they express IL-10, TGFβ, and TNFα [10]. TNF-α is produced by all CD4+ T cells [11,[72][73][74][75]. IL-10 inhibits macrophages and Th1 cell proliferation [76,77].…”

Section: T-helper Lymphocyte-2 Cellsmentioning

confidence: 99%

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Immunogenetic contributions to recurrent pregnancy loss

Grimstad

Krieg

2016

J Assist Reprod Genet

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“…However, it was shown that with the stopping of the embryo development the concentration and ratio of pro and antiinflammatory cytokines (particularly, TNFα and IL10) in the peripheral blood of women and in the chorionic villi depend on the embryo kary otype (Calleja Agius et al, 2012). The authors assume the existence of different mechanisms for the elimina tion of embryos with a normal and abnormal karyo type.…”

Section: Discussionmentioning

confidence: 99%

Cytokine gene polymorphisms and early pregnancy loss

Машкина

Коваленко

Фомина

et al. 2015

Russ J Genet Appl Res

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A disbalance of pro and antiinflammatory cytokines can negatively affect the early stages of human embryogenesis. The association between polymorphism of cytokine genes (-31C T IL1β, -174G C IL6, -308G A TNFα, and -592C A and -819C T IL10) and pregnancy loss was studied. The analysis was performed on DNA samples from two groups of women with pregnancy loss: those with a missed abortion (MA) (n = 62) and those with a spontaneous abortion (SA) (n = 62). The control group included 114 women with normal pregnancy. Cytokine genotyping was performed using PCR with sequence specific primers with the CNP express kit (Lytech, Russian Federation). The increase in the frequency of heterozygotes for the -31C T polymorphism of the IL1β gene among women with MA (58.1%) compared to those with SA (36.7%) was found. In the SA group, the frequency of heterozygotes for -591C T of the IL10 gene was higher (56.7%) than in the control group (32.5%). The frequency of the -819T allele of IL10 gene among women with SA was higher than in the control group (0.33 vs 0.23). At the same time, the frequency of the -308A allele of the TNFα gene was the lowest in the SA group compared to those in the MA and the control group. Our data show that the risk of spontaneous abortion increases if the -592A and -819T alleles of the IL10 and -308G allele of TNFα are present in the genotype.

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Deficiency of monoclonal non‐specific suppressor factor beta (MNSFB) promotes pregnancy loss in mice

Zhang

et al. 2015

Molecular Reproduction Devel

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Maternal immune tolerance to the semi-allogenic fetus is required for successful pregnancy in mammals. Monoclonal nonspecific suppressor factor beta (MNSFB) is an immunosuppressive factor present in uterine epithelial and stromal cells, as well as in macrophages and T cells. Although the functional neutralization of MNSFB using specific antibodies against it lead to failed embryo implantation in mice, the exact role of MNSFB at the fetal-maternal interface remains unclear. The present study generated conditional heterozygous Mnsfb-deficient (Mnsfb(+/) (-) ) mice using the LoxP/Cre system. Western-blot analyses showed that uterine MNSFB protein in Mnsfb(+/-) mice was remarkably down-regulated compared to that in the wild-type (Mnsfb(+/+) ) mice. The litter size of female Mnsfb(+/-) mice was significantly reduced, which corresponded to developmental failure of embryos beyond Day 11 of pregnancy. The expression level of MNSFB protein was also lower in the failing compared to the normal embryos. An aberrant interaction between the embryos of Day-4 pregnant wild-type mice and endometrial stromal cells of female Mnsfb(+/-) mice was observed in vitro. The uterine Day-5 abundance of P53, BAX, and BCL-G in pregnant Mnsfb(+/-) mice was significantly decreased compared to that of wild-type mice, whereas the expression of P27 and tumor necrosis factor alpha (TNFA) was elevated. By comparison, the levels of MNSFB and BAX proteins in human decidual tissues obtained from recurrent spontaneous miscarriage patients were significantly reduced compared to those obtained from legal medial abortion, highlighting the involvement of MNSFB in the pathogenesis of recurrent spontaneous miscarriage. Together, these results demonstrated that a deficiency in MNSFb is associated with pregnancy loss, probably through reduced P53 and/or increased TNFA production at the fetal-maternal interface.

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Placental Villous Expression of TNFα and IL‐10 and Effect of Oxygen Tension in Euploid Early Pregnancy Failure

Abstract: Increased levels of TNFα and decreased levels of receptors in miscarriage villous tissue confirm an excessive placental inflammation in miscarriage patients.

Cited by 15 publications

References 58 publications

Immunogenetic contributions to recurrent pregnancy loss

Immunogenetic contributions to recurrent pregnancy loss

Cytokine gene polymorphisms and early pregnancy loss

Deficiency of monoclonal non‐specific suppressor factor beta (MNSFB) promotes pregnancy loss in mice

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