4 Immune aspects of pathology of the placental bed contributing to pregnancy pathology

Bulmer, Judith N.

doi:10.1016/s0950-3552(05)80006-9

Cited by 56 publications

(28 citation statements)

References 90 publications

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“…Several pathologic conditions can lead to IUGR, some of which have been related to the risk for testicular cancer, such as immunological defects, placental insufficiency, maternal anemia, renal disease and birth defects. 31,46,47 Low birth weight (especially being small for gestational age) is associated with cryptorchidism, which is the best established risk factor of etiologic significance for testicular cancer. 39,48,49 Lower birth weight is also related to twinning and early delivery.…”

Section: Discussionmentioning

confidence: 99%

Birth weight and the risk of testicular cancer: A meta‐analysis

Michos

Xue

Michels

2007

Intl Journal of Cancer

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The high incidence of testicular cancer in young males indicates a potential role of events during early life. Birth weight has been identified as a factor possibly associated with the risk of cancers later in life. To investigate the association between birth weight and testicular cancer, we conducted a Systematic Review and Meta-Analysis of published studies investigating the association between birth weight and testicular cancer. Data were combined using a fixed-effects model. Thirteen epidemiologic studies, published between 1983 and 2004, were included in the analysis, encompassing 5,663 patients with testicular cancer. Men weighing less than 2,500 grams at birth had a higher risk for developing testicular cancer later in life than those with normal birth weight (2,500-4,000 g) (OR 5 1.18; 95% confidence interval (CI) 1.01-1.38). A similar trend was found for men with a birth weight above 4,000 g, (OR 5 1.12; 95% CI 1.02-1.22). When seminoma and nonseminoma testicular cancer cases were considered separately, low birth weight was a risk factor specifically for seminomas (OR 5 1.44; 95% CI 1.11-1.88). A U-shaped association was observed between birth weight and the risk for testicular cancer. The underlying biological mechanisms for this phenomenon remain to be elucidated. ' 2007 Wiley-Liss, Inc.Key words: testicular cancer; birth weight; risk factors Testicular cancer is the most common cancer among young male adults, with a peak incidence among men aged 25-35 years and with a distinctive geographical and racial variation. The incidence varies 10-fold among countries, with the highest among white men in Northern Europe. 1 The incidence increased by 51% in the United States from 1973 to 1995, though it stabilized in the first half of the 1990s.2,3 An increase in incidence has been reported from other countries. 4,5 These data suggest that both genetic and environmental factors are important for the development of testicular tumors.Most testicular cancers are germ cell tumors (GCTs), with 50% being seminomas and the remaining 50% nonseminomas. 6 Nonseminomas often represent tumors of mixed histology and may include a variety of seminoma or nonseminoma histologic subtypes. The International Agency for Research on Cancer (IARC) and the WHO classify testicular GCTs into 3 types: the teratomas and yolk-sac tumors of newborns and infants; the seminomatous and nonseminomatous tumors of adolescents and young adults; and the spermatocytic seminomas of the elderly.7 Further classification beyond the 2 main histologic categories (seminomas and nonseminomas) appears to have limited relevance in etiologic or clinical settings. 8,9 Given the age incidence pattern of testicular cancer, which peaks in the third decade of life, etiologic research has focused on prenatal, perinatal and early-life exposures. A number of different factors have been identified that predispose men to testicular cancer. Cryptorchidism is the only established risk factor of etiologic significance, but it accounts for fewer than 10% of all cases. 10...

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Section: Discussionmentioning

confidence: 99%

Birth weight and the risk of testicular cancer: A meta‐analysis

Michos

Xue

Michels

2007

Intl Journal of Cancer

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“…Insufficient acquiescence by the maternal immune system may lead to the inadequate placentation of recurrent pregnancy loss, intrauterine growth restriction, and preeclampsia (1). Overzealous fetal invasion may lead to morbid adherence of the placenta, placenta accreta, increta, and percreta (2).…”

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confidence: 99%

Decidual NK Cells Alter In Vitro First Trimester Extravillous Cytotrophoblast Migration: A Role for IFN-γ

Dutz

MacCalman

et al. 2006

The Journal of Immunology

124

110

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Abnormal placentation results in either inadequate (consequences: recurrent miscarriage, intrauterine growth restriction, and preeclampsia) or overzealous (consequences: placenta accreta, increta, and percreta) placentation. NK cells dominate in first trimester decidua and probably control extravillous cytotrophoblast (EVT) invasion. We examined this interaction in a novel way, using NK cells and villous explants from concordant first trimester pregnancies cocultured using a new collagen (two-dimensional) model of placentation. Decidual NK (dNK) cells exerted contact-independent inhibition of normal cytotrophoblast migration, associated with changes in the cytotrophoblast expression of metalloproteases-2 and -9, and plasminogen activator inhibitor-1. dNK cells did not affect EVT proliferation and apoptosis, and cell column formation. dNK cell effects were partially reversed by neutralizing Abs against IFN-γ. We provide ex vivo human evidence of a direct role for dNK in modulating EVT differentiation as they form columns and then migrate from anchoring villi.

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“…In addition, trophoblasts themselves possess certain properties that could promote tolerance. These include a lack of MHC antigen expression (12), the presence of immunosuppressive substances such as transforming growth factor-␤ (13), and the expression of CD59, an inhibitor of the complement cascade (14).…”

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confidence: 99%

Fas and Fas Ligand Expression in Maternal Blood and in Umbilical Cord Blood in Preeclampsia

et al. 2001

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The Fas-Fas ligand (FasL) pathway of apoptosis is abnormally activated in diseases associated with impaired immune tolerance or chronic inflammation. Pregnancy-related hypertension is a spectrum of disease that commonly causes significant morbidity in women and in their newborn infants, is associated with generalized inflammation, and may be causally related to impaired maternal-fetal tolerance. Our recent observation of enhanced trophoblast expression of FasL in one form of pregnancy-related hypertension led us to hypothesize that this group of disorders might be associated with abnormal activation of the Fas-FasL pathway. To test this hypothesis, we prospectively quantified soluble and leukocyte-associated Fas receptor and FasL in the maternal and umbilical cord blood (CB) sera of 20 gestations complicated by preeclampsia and of 18 normal control gestations, using ELISA and flow cytometric analyses. We determined higher soluble FasL levels in paired maternal and CB sera of hypertensive gestations compared with control gestations (p Ͻ 0.01); in contrast, soluble Fas levels were similar between groups. Surface expression of FasL was lower on maternal (p Ͻ 0.01) and CB (p Ͻ 0.05) neutrophils from affected gestations, whereas surface Fas expression was lower on maternal (p Ͻ 0.02), but not CB, neutrophils and lymphocytes. We conclude that expression of Fas and FasL in sera and on leukocytes is altered in gestations complicated by preeclampsia, and speculate that activation of the Fas-FasL pathway mediates associated pathologic processes in affected women and in their neonates. Activation of the Fas-Fas Ligand pathway involves cellular interactions between the Fas receptor and FasL, and can result in apoptosis or in an inflammatory response (1). The Fas receptor (CD95, Apo-1, FasR), a type I integral membrane protein belonging to the tumor necrosis factor receptor family, is expressed on numerous cell types including hematopoietic cells, and its expression increases during inflammation (1). In contrast, expression of FasL (CD95L), a type II transmembrane molecule belonging to the tumor necrosis factor receptor superfamily, is limited to certain leukocytes and tissues with immune privilege (2). Fas-FasL interactions leading to clonal deletion of antigen-presenting cells have been implicated in the establishment of graft tolerance (3), and provide one explanation for the immune privilege status of certain tissues, including the placenta, cornea, and testis (2). In contrast, abnormal function of the Fas-FasL pathway is involved in the pathogenesis of a variety of disorders, including cytopenias, autoimmune diseases, graft-versus-host disease, and graft rejection (1,(3)(4)(5)(6).Mice with the gld mutation are deficient in FasL function and have smaller litters with decreased viability (7). Studies in these mice suggest that the Fas-FasL pathway contributes to preservation of the fetal allograft by preventing the trafficking of activated leukocytes between the mother and fetus during normal gestation, observations also ...

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4 Immune aspects of pathology of the placental bed contributing to pregnancy pathology

Cited by 56 publications

References 90 publications

Birth weight and the risk of testicular cancer: A meta‐analysis

Birth weight and the risk of testicular cancer: A meta‐analysis

Decidual NK Cells Alter In Vitro First Trimester Extravillous Cytotrophoblast Migration: A Role for IFN-γ

Fas and Fas Ligand Expression in Maternal Blood and in Umbilical Cord Blood in Preeclampsia

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