T-Helper 1-Type Immunity to Trophoblast in Women With Recurrent Spontaneous Abortion

Hill, Joseph A.; Polgár, Katalin; Anderson, Deborah J.

doi:10.1001/jama.1995.03520480053039

Cited by 423 publications

(159 citation statements)

References 34 publications

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“…The increasing trend of TNFα/IL-10 ratio from nonpregnant to pregnant then eclamptic patients indicates that IL-10 is necessary as a beneficial balance to the adverse effects of the inflammatory cytokine cascade in eclampsia. This is similar to the study by Hill et al, [21] where trophoblast activated lymphocyte supernatants from reproductively normal women contained IL-10 and IL-4, while supernatants from women with unexplained recurrent abortions (URA) had predominantly TNF-α. It was their view that whereas TH1 type immunity to trophoblast was associated with URA and might play a role in reproductive failure, TH2 type immunity may be a natural response to trophoblast contributing to successful pregnancy.…”

Section: Discussionsupporting

confidence: 90%

Serum cytokine levels and T lymphocyte subsets in pregnant women with eclampsia

Musa¹,

Onyemelukwe²,

Olatunji³

et al. 2012

OJI

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Background: Eclampsia, defined as the occurrence during pregnancy of hypertension, oedema, proteinuria and/or other neurologic abnormalities, causes substantial morbidity and mortality for both mother and foetus. However, its aetiology is largely unknown. Genetic and immune factors may play a role including a reduced maternal response to paternal antigen and an altered adaptation of the maternal immune system to the foetus. Methods: Participants consisted of pregnant women with and without a diagnosis of eclampsia (N = 20, each group), and normal healthy nonpregnant controls (N = 18). Women with smear positive malaria or clinical infections were excluded. Serum levels of TNFα and IL-10 were assayed by ELISA. T lymphocyte subsets of pregnant patients with and without eclampsia were also studied by direct immunofluorescence using monoclonal antibodies and compared with the control group of 18 normal healthy nonpregnant women (NHC). Results: Eclampsia was associated with significantly lower mean serum IL-10 levels compared to normal pregnant and nonpregnant controls. Levels of the pro-inflammatory cytokine TNFα were higher in pregnant women with and without eclampsia, compared to control nonpregnant women. Further differences on serum cytokine levels were observed in the significantly increasing ratio of IL-10 to TNFα from nonpregnant controls to normal pregnant women and to pregnant women with eclampsia. The mean values of CD3+ and CD4+ positive lymphocytes was significantly decreased in patients with eclampsia (p < 0.05) in this study compared to pregnant controls. Similarly, CD3+ and CD4+ T cells were further decreased in eclampsia and pregnant controls compared to nonpregnant controls (p < 0.05). A decreasing CD4/CD8 ratio was observed from non-pregnant to pregnant controls and to patients with eclampsia buttressing an increase in CD8+ cells in eclampsia and pregnancy compared to controls. Conclusions: While a pro-inflammatory immune milieu during pregnancy complicated with eclampsia was demonstrated, the presence of eclampsia was not associated with further cytokine differences.

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Section: Discussionsupporting

confidence: 90%

Serum cytokine levels and T lymphocyte subsets in pregnant women with eclampsia

Musa¹,

Onyemelukwe²,

Olatunji³

et al. 2012

OJI

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“…In both mice and man, failure to shift from Th1 to Th2 mediated immunity in pregnancy results in an increase in spontaneous abortion (Hill et al, 1995, Krishnan et al, 1996a, Lin et al, 1993). This shift in immune response from Th1 to Th2 occurs both locally at the maternal fetal interface (Lin et al, 1993, Sacks et al, 2001, Wegmann et al, 1993) as well as systemically (Dudley et al, 1993, Elenkov et al, 2001, Fabris et al, 1977, Hill et al, 1995, Krishnan et al, 1996b, Marzi et al, 1996).…”

Section: Resultsmentioning

confidence: 99%

“…This shift in immune response from Th1 to Th2 occurs both locally at the maternal fetal interface (Lin et al, 1993, Sacks et al, 2001, Wegmann et al, 1993) as well as systemically (Dudley et al, 1993, Elenkov et al, 2001, Fabris et al, 1977, Hill et al, 1995, Krishnan et al, 1996b, Marzi et al, 1996). The systemic shift away from Th1 and toward Th2 was initially shown in murine systems by a decrease in mixed lymphocyte reactions of splenocytes and an increase in antibody production during pregnancy (Fabris et al, 1977).…”

Section: Resultsmentioning

confidence: 99%

The immunologic effects of estrogen on psoriasis: A comprehensive review

Danesh

Murase

2015

International Journal of Women's Dermatology

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BackgroundImmunological changes in pregnancy are associated with improvements in some pre-existing immune-mediated skin diseases. Estrogen has been hypothesized to contribute to these changes by creating a shift from Th1 and Th17 to Th2 immunity. As this hypothesis would predict, psoriasis (a primarily Th17 mediated immune disease) tends to improve during pregnancy. However, the precise mechanism by which estrogen induces immunological change in psoriasis remains poorly understood.ObjectiveTo summarize the immunologic effects of estrogen as they relate to psoriasis during pregnancy.MethodsWe performed an English-language PubMed search of articles from September 2004 to September 2014 combining the key terms "psoriasis," "estrogen," "autoimmune disease," and "pregnancy."ResultsEstrogen appears to up-regulate Th2 cytokines and down-regulate Th1 and Th17 cytokines. This shift was initially observed in murine systems, which showed decreased mixed lymphocyte reactions of splenocytes and increased antibody production during pregnancy. Antigen stimulated splenocytes produced fewer Th1 cytokines and more Th2 cytokines in pregnant mice. IL17 producing T cells were significantly decreased in healthy pregnancies compared to non-pregnant controls.LimitationsThis review is limited by the paucity of studies evaluating immunological changes of psoriasis in pregnancy among human subjects.ConclusionsIncreased estrogen production in pregnancy is associated with decreased Th1 and Th17 cytokine production. While estrogen may be responsible for some of these immune shifts resulting in disease improvement, there remains no definitive evidence to prove the hypothesis that estrogen is responsible for such improvement.

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“…For example, serum taken from women suffering from recurrent spontaneous abortion have a cytokine profile indicative of a Th1 response compared to healthy pregnant women. 168 To counter this, intravenous immunoglobin (IVIG) given to women, with reported previous recurrent miscarriages and/or suffering from recurrent miscarriages after IVF, every 3–4 weeks starting from conception or 24 hours before embryo transfer showed a decrease of natural killer cells and a implantation success rate of 92.5%,compared to 25% for women not receiving IVIG. 169 Moreover, new immunotherapies for promoting tolerance to the fetus during gestation are being studied in animal models and could have important implications in melanoma.…”

Section: Reversing Tolerance In Melanomamentioning

confidence: 99%

Immunomodulatory Effects of Sex Hormones: Requirements for Pregnancy and Relevance in Melanoma

Enninga

Holtan

Creedon

et al. 2014

Mayo Clinic Proceedings

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Similarities between the pathologic progression of cancer and the physiologic process of placentation (e.g., proliferation, invasion, and local/systemic tolerance) have been recognized for many years. Sex hormones such as human chorionic gonadotropin, estrogens, progesterone, and others contribute to induction of immunologic tolerance at the beginning of gestation. Sex hormones have been shown to play contributory roles in the growth of cancers such as breast, prostrate, endometrial and ovarian cancer, but their involvement as putative mediators of the immunologic escape of cancer are still being elucidated. Herein, we compare the emerging mechanism by which sex hormones modulate systemic immunity in pregnancy and their potentially similar role in cancer. To do this, we conducted a PubMed search using combinations of the following key words: immune regulation, sex hormones, pregnancy, melanoma and cancer. We did not limit our search to specific publication dates. Mimicking the maternal immune response to pregnancy, especially in late gestation, might aid in design of better therapies to reconstitute endogenous anti-tumor immunity and improve survival.

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T-Helper 1-Type Immunity to Trophoblast in Women With Recurrent Spontaneous Abortion

Abstract: Whereas TH1-type immunity to trophoblast is associated with URA and may play a role in reproductive failure, TH2-type immunity may be a natural response to trophoblast contributing to successful pregnancy.

Cited by 423 publications

References 34 publications

Serum cytokine levels and T lymphocyte subsets in pregnant women with eclampsia

Serum cytokine levels and T lymphocyte subsets in pregnant women with eclampsia

The immunologic effects of estrogen on psoriasis: A comprehensive review

Immunomodulatory Effects of Sex Hormones: Requirements for Pregnancy and Relevance in Melanoma

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