Indoleamine 2,3-dioxygenase (IDO) expression in invasive extravillous trophoblast supports role of the enzyme for materno-fetal tolerance

Hönig, Arnd; Rieger, Lorenz; Kapp, Michaela; Sütterlin, Marc; Dietl, Johannes; Kämmerer, Ulrike

doi:10.1016/j.jri.2003.11.002

Cited by 130 publications

(100 citation statements)

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“…CTLA-4-expressing nT reg are present in high numbers in the decidua [70,71]. They may be crucial in the high IDO level detected at the fetal-maternal interface, which has been proposed as a major factor in the lower immune reactivity of this compartment [71][72][73][74][75].…”

Section: Natural Treg In Neonatesmentioning

confidence: 99%

Defective antigen-presenting cell function in human neonates

Velilla¹,

Rugeles²,

Chougnet³

2006

Clinical Immunology

152

132

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Immaturity of the immune system has been suggested as an underlying factor for the high rate of morbidity and mortality from infections in newborns. Functional impairment of neonatal T cells is frequently quoted as the main underlying mechanism for such immaturity. However, recent studies suggest that neonatal antigen-presenting cells (APCs) also exhibit functional alterations, which could lead to secondary defects of adaptive T cell responses. In this review, we summarize what is known on the functionality of APC at birth and during early childhood. Compared to adults, neonatal APCs display markers of immaturity and produce low levels of cytokines. Multiple factors could be involved in neonatal APC alteration, such as intrinsic immaturity, defective interaction between APCs and T cells, and regulatory T cell-mediated inhibition. Characterization of the relative contribution of each mechanism is clearly needed to better understand the functional capability of the neonatal immune system.

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Section: Natural Treg In Neonatesmentioning

confidence: 99%

Defective antigen-presenting cell function in human neonates

Velilla¹,

Rugeles²,

Chougnet³

2006

Clinical Immunology

152

132

View full text Add to dashboard Cite

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“…17,18 Conversely, others have found that IDO was only present in subtrophoblastic capillaries of the placental villi of first trimester pregnancies. [19][20][21] Ho¨nig et al 22 demonstrated that the invasive evCTs were strongly positive for IDO, but that syncytiotrophoblasts were negative in the first trimester of pregnancy. Moreover, IDO was localized to the decidual glandular epithelium, decidual stromal cells, monocytes or 'lineage negative, human leucocyte antigen D-related positive dendritic cells' according to numerous studies.…”

Section: Introductionmentioning

confidence: 99%

Indoleamine 2,3-dioxygenase levels at the normal and recurrent spontaneous abortion fetal–maternal interface

et al. 2013

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Objectives: To localize indoleamine 2,3-dioxygenase (IDO) mRNA and protein and to undertake a functional study at the first trimester fetal-maternal interface in order to determine whether the distribution and function of IDO are related to recurrent spontaneous abortion (RSA). Methods: Women undergoing legal pregnancy termination and women with RSA participated in this prospective study. Immunohistochemistry and real-time reverse transcription-polymerase chain reaction were used to analyse levels of IDO protein and mRNA in placenta, decidua and HTR-8/SVneo cells. Culture medium collected from trophoblast villous explant or HTR-8/SVneo cell cultures was used to measure IDO activity in response to interferon (IFN)-g treatment. Results: A total of 40 healthy women and 26 women with RSA provided samples of placenta and decidua. For normal pregnancies, IDO protein and mRNA was identified in placental trophoblasts, invasive extravillous trophoblasts and decidual glandular epithelium. IFN-g significantly increased IDO activity in trophoblast villous explants and HTR-8/SVneo cells. Levels of IDO protein and mRNA in the placenta and decidua from normal pregnancies were significantly higher than in those from RSA. Conclusions: Decreased levels of IDO protein and mRNA in the placenta and decidua from RSA suggest an important role for IDO in the maintenance of normal pregnancy.

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“…5 IDO is expressed by human extravillous trophoblast cells and is constitutively active at the maternal-fetal interface. 6,7 Primary trophoblast giant cells of fetal origin express IDO and an IDO inhibitor induced pregnant mice to undergo immune rejection of allogeneic embryos. [8][9][10] In inflammatory bowel disease, inhibition of IDO results in marked exacerbation Indolamine-2,3-dioxygenase (IDO) is expressed in tumor antigen presenting cells (apCs) and plays an important role in tumor immune tolerance.…”

Section: Introductionmentioning

confidence: 99%