The Effect of Trophoblasts on T Lymphocytes: Possible Regulatory Effector Molecules - A Proteomic Analysis

Dong, Minyue; Ding, Guo‐Lian; Zhou, Jun; Wang, Hanzhi; Zhao, Yi; Huang, He‐Feng

doi:10.1159/000129639

Cited by 55 publications

(41 citation statements)

References 59 publications

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“…However, these cytotrophoblast preparations also contained CD34 mRNA (Cvitic and Desoye, personal communication), so that contamination with endothelial cells cannot be excluded. Contaminating endothelial cells may also explain similar findings reported earlier by Dong et al (68). In mice, placental IDO1 expression was found to be limited to trophoblast giant cells (69).…”

Section: Placental Expression and Localization Of Trp-degrading Enzymessupporting

confidence: 89%

The Role of Placental Tryptophan Catabolism

2014

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This review discusses the mechanisms and consequences of degradation of tryptophan (Trp) in the placenta, focusing mainly on the role of indoleamine 2,3-dioxygenase-1 (IDO1), one of three enzymes catalyzing the first step of the kynurenine pathway of Trp degradation. IDO1 has been implicated in regulation of feto-maternal tolerance in the mouse. Local depletion of Trp and/or the presence of metabolites of the kynurenine pathway mediate immunoregulation and exert antimicrobial functions. In addition to the decidual glandular epithelium, IDO1 is localized in the vascular endothelium of the villous chorion and also in the endothelium of spiral arteries of the decidua. Possible consequences of IDO1-mediated catabolism of Trp in the endothelium encompass antimicrobial activity and immunosuppression, as well as relaxation of the placental vasotonus, thereby contributing to placental perfusion and growth of both placenta and fetus. It remains to be evaluated whether other enzymes mediating Trp oxidation, such as indoleamine 2,3-dioxygenase-2, Trp 2,3-dioxygenase, and Trp hydroxylase-1 are of relevance to the biology of the placenta.

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Section: Placental Expression and Localization Of Trp-degrading Enzymessupporting

confidence: 89%

The Role of Placental Tryptophan Catabolism

2014

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“…These complex immune interactions between the mother and the fetus are conveyed by cell membrane- and vesicle-bound as well as soluble molecules. Among the best studied molecular mechanisms are the effect of progesterone-induced blocking factor (PIBF) on the shift towards Th2 over Th1 cytokine production (131), the anti-inflammatory role of decidual macrophages (132), the immunosuppressive effects of decidual galectin-1 (16), trophoblastic indoleamine 2,3-dyoxignease (IDO), FAS/FAS ligand and galectin-1 (133, 134), and the roles of human leukocyte antigen (HLA)-C and HLA-G in protecting fetal cells from NK- and cytotoxic lymphocyte (CTL)-mediated cytolysis (135, 136). It is a question for future studies how the actions of PP13 are related to this complex, dynamically changing cellular and molecular network during placentation.…”

Section: In Vitro and In Vivo Functional Studies On Pp13mentioning

confidence: 99%

Placental Protein 13 (PP13) â€“ A Placental Immunoregulatory Galectin Protecting Pregnancy

et al. 2014

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Galectins are glycan-binding proteins that regulate innate and adaptive immune responses, and some confer maternal-fetal immune tolerance in eutherian mammals. A chromosome 19 cluster of galectins has emerged in anthropoid primates, species with deep placentation and long gestation. Three of the five human cluster galectins are solely expressed in the placenta, where they may confer additional immunoregulatory functions to enable deep placentation. One of these is galectin-13, also known as Placental Protein 13 (PP13). It has a “jelly-roll” fold, carbohydrate-recognition domain and sugar-binding preference resembling other mammalian galectins. PP13 is predominantly expressed by the syncytiotrophoblast and released from the placenta into the maternal circulation. Its ability to induce apoptosis of activated T cells in vitro, and to divert and kill T cells as well as macrophages in the maternal decidua in situ, suggests important immune functions. Indeed, mutations in the promoter and an exon of LGALS13 presumably leading to altered or non-functional protein expression are associated with a higher frequency of preeclampsia and other obstetrical syndromes, which involve immune dysregulation. Moreover, decreased placental expression of PP13 and its low concentrations in first trimester maternal sera are associated with elevated risk of preeclampsia. Indeed, PP13 turned to be a good early biomarker to assess maternal risk for the subsequent development of pregnancy complications caused by impaired placentation. Due to the ischemic placental stress in preterm preeclampsia, there is increased trophoblastic shedding of PP13 immunopositive microvesicles starting in the second trimester, which leads to high maternal blood PP13 concentrations. Our meta-analysis suggests that this phenomenon may enable the potential use of PP13 in directing patient management near to or at the time of delivery. Recent findings on the beneficial effects of PP13 on decreasing blood pressure due to vasodilatation in pregnant animals suggest its therapeutic potential in preeclampsia.

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“…IDO depletes L-tryptophan, inhibiting T-cell proliferation, and is highly expressed on EVT (Honig et al 2004). IDO may also be released by trophoblast, as conditioned media derived from trophoblast or villous explant cultures inhibit T-cell proliferation, while inhibiting IDO or adding tryptophan partly restored T-cell proliferation (Dong et al 2008).…”

Section: Ido and Immune Suppressionmentioning

confidence: 99%

A balancing act: mechanisms by which the fetus avoids rejection by the maternal immune system

Warning¹,

McCracken²,

Morris³

2011

Reproduction

212

139

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Successful pregnancy requires strict temporal regulation of maternal immune function to accommodate the growing fetus. Early implantation is facilitated by inflammatory processes that ensure adequate vascular remodeling and placental invasion. To prevent rejection of the fetus, this inflammation must be curtailed; reproductive immunologists are discovering that this process is orchestrated by the fetal unit and, in particular, the extravillous trophoblast. Soluble and particulate factors produced by the trophoblast regulate maternal immune cells within the decidua, as well as in the periphery. The aim of this review is to discuss the action of recently discovered immunomodulatory factors and mechanisms, and the potential effects of dysregulation of such mechanisms on the maternal immune response that may result in pregnancy loss or preeclampsia.

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The Effect of Trophoblasts on T Lymphocytes: Possible Regulatory Effector Molecules - A Proteomic Analysis

Cited by 55 publications

References 59 publications

The Role of Placental Tryptophan Catabolism

The Role of Placental Tryptophan Catabolism

Placental Protein 13 (PP13) â€“ A Placental Immunoregulatory Galectin Protecting Pregnancy

A balancing act: mechanisms by which the fetus avoids rejection by the maternal immune system

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