Inadequate tolerance induction may induce pre-eclampsia

Saito, Shigeru; Sakai, Masatoshi; Sasaki, Yasushi; Nakashima, Akitoshi; Shiozaki, Arihiro

doi:10.1016/j.jri.2007.08.002

Cited by 97 publications

(80 citation statements)

References 50 publications

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“…Furthermore, there may be partner specificity, 7 which strengthens the argument that pre-eclampsia results from a relative failure to induce maternal tolerance of paternal alloantigens. 8 Partners, Coitus, Sperm, and Semen A change of partner seems to restore the risk of preeclampsia to that of primiparity in multigravid women, for example Zhang and Patel 2007. 9 But, a change of partner is also associated with a long inter-pregnancy interval.…”

Section: Clinical and Epidemiological Considerationsmentioning

confidence: 99%

REVIEW ARTICLE: Immunology of Pre‐Eclampsia

Redman

Sargent

2010

American J Rep Immunol

612

486

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Citation Redman CWG, Sargent IL. Immunology of Pre‐eclampsia. Am J Reprod Immunol 2010Pre‐eclampsia develops in stages, only the last being the clinical illness. This is generated by a non‐specific, systemic (vascular), inflammatory response, secondary to placental oxidative stress and not by reactivity to fetal alloantigens. However, maternal adaptation to fetal (paternal alloantigens) is crucial in the earlier stages. A pre‐conceptual phase involves maternal tolerization to paternal antigens by seminal plasma. After conception, regulatory T cells, interacting with indoleamine 2,3‐dioxygenase, together with decidual NK cell recognition of fetal HLA‐C on extravillous trophoblast may facilitate placental growth by immunoregulation. Complete failure of this mechanism would cause miscarriage, while partial failure would cause poor placentation and dysfunctional uteroplacental perfusion. The first pregnancy preponderance and partner specificity of pre‐eclampsia can be explained by this model. For the first time, the pathogenesis of pre‐eclampsia can be related to defined immune mechanisms that are appropriate to the fetomaternal frontier. Now, the challenge is to prove the detail.

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Section: Clinical and Epidemiological Considerationsmentioning

confidence: 99%

REVIEW ARTICLE: Immunology of Pre‐Eclampsia

Redman

Sargent

2010

American J Rep Immunol

612

486

View full text Add to dashboard Cite

show abstract

“…In a large proportion of pregnancies, the maternal immune response is less than adequately regulated and inflammation and immunity develop to varying degrees. Insufficient Tregs, associated with more prevalent Th1 and Th17 cells that react with fetal allo-antigens, are linked with pregnancy disorders and conditions including preeclampsia, fetal growth restriction and spontaneous preterm birth [38]. …”

Section: Gestational Exposuresmentioning

confidence: 99%

In utero Programming of Allergic Susceptibility

Grieger

Clifton

Tuck

et al. 2016

Int Arch Allergy Immunol

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Background: Around 30-40% of the world's population will experience allergy, the most common and earliest-onset noncommunicable disease. With a steady rise in the incidence of allergic disease over recent decades, up to 18% of children will suffer a respiratory, food or skin allergy before their 18th birthday. There is compelling evidence that the risk of developing allergy is influenced by early life events and particularly in utero exposures. Methods: A comprehensive literature review was undertaken which outlines prenatal risk factors and potential mechanisms underlying the development of allergy in childhood. Results: Exposures including maternal cigarette smoking, preterm birth and Caesarean delivery are implicated in predisposing infants to the later development of allergy. In contrast, restricted growth in utero, a healthy maternal diet and a larger family size are protective, but the mechanisms here are unclear and require further investigation. Conclusion: To ameliorate the allergy pandemic in young children, we must define prenatal mechanisms that alter the programming of the fetal immune system and also identify specific targets for antenatal interventions.

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“…Trophoblast cells have particular characteristics as to the expression of HLA molecules (Human Leukocitary Antigen). They express only HLA-G, HLA-C and HLA-E. Saito, Sakai, Sasaki, Nakashima and Shiozaki (2007) demonstrated reduction in the percentage of regulatory T cells in patients with preeclampsia; this would lead to increased activation of lymphocytes and thus, greater inflammatory response. Therefore, one can infer that the breakdown of maternal-fetal or maternal-placental tolerance could lead to deficient placentation, inflammatory response and, consequently, to preeclampsia (Oliveira, Karumanchi, & Sass, 2010).…”

Section: Immunohistochemistry (Ihc)mentioning

confidence: 97%

<b>Expression of bradykinin in human placenta from healthy and preeclamptic women

Oliveira

Pereira

Bertevello

et al. 2017

Acta Sci. Health Sci.

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ABSTRACT. This study evaluated the expression of bradykinin (BK) in human placenta from healthy and preeclamptic women. This is a non-randomized experimental study, in which we performed histological analysis of placental tissue to observe changes that occur in each kind of placenta as well as immunohistochemical analysis to investigate the expression of bradykinin. We used 'Paleontological Statistics software package for education and data analysis' 3.06 and R for the statistical analysis. The Ethics Committee of the University of Rio Grande do Norte State approved this experiment under protocol number 166370, according to the determinations established by Resolutions 466/12 and 441/11.We found differences between the two kinds of placenta concerning the diameter of the vessels and the rate of cytotrophoblastic invasion. Student's t-test evidenced significant difference (p = 7.6395 x 10 -5 ) indicating greater marking of BK per section in the healthy placenta group. The result of more significant expression of bradykinin in healthy placenta can be used as a starting point for deeper researches aiming to better characterize and quantify this expression.Keywords: gynecology, obstetrics, immunohistochemistry.Expressão de bradicinina em placentas humanas saudáveis e pré-eclâmpticas RESUMO. Este estudo avaliou a expressão de bradicinina em placentas humanas saudáveis e pré-eclâmpticas. Trata-se de um estudo de caráter experimental não randomizado, no qual foi feita uma análise histológica dos tecidos placentários, permitindo a observação das alterações ocorridas em cada tipo de placenta, e a técnica de imuno-histoquímica, a fim de investigar a presença de bradicinina. Foi utilizado o Paleontological Statistics software package for education and data analysis 3.06 para a análise estatística. Este estudo foi aprovado pelo Comitê de Ética da Universidade do Estado do Rio Grande do Norte sob o protocolo número 166.370, de acordo com as diretrizes estabelecidas nas Resoluções 466/12 e 441/11. Foi possível observar diferenças no diâmetro dos vasos e na invasão citotrofoblástica entre os dois tipos de placentas. O teste t de Student mostrou significância estatística (p = 7,6395 x 10 -5 ) para uma maior marcação de BK por secção no grupo de placentas saudáveis. O resultado obtido com relação à expressão mais significante de bradicinina em placentas saudáveis pode ser visto como precursor de uma pesquisa mais aprofundada, para melhor caracterizar e quantificar essa expressão.Palavras-chave: ginecologia, obstetrícia, imuno-histoquímica.

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Inadequate tolerance induction may induce pre-eclampsia

Cited by 97 publications

References 50 publications

REVIEW ARTICLE: Immunology of Pre‐Eclampsia

REVIEW ARTICLE: Immunology of Pre‐Eclampsia

In utero Programming of Allergic Susceptibility

<b>Expression of bradykinin in human placenta from healthy and preeclamptic women

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