Pregnancy specific glycoprotein 18 induces IL-10 expression in murine macrophages

Wessells, Jennifer; Wessner, David R.; Parsells, Roseann; White, Kimberly A.; Finkenzeller, Daniela; Zimmermann, Wolfgang; Dveksler, Gabriela S.

doi:10.1002/1521-4141(200007)30:7<1830::aid-immu1830>3.0.co;2-m

Cited by 62 publications

(57 citation statements)

References 29 publications

(33 reference statements)

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“…Pregnancy-specific glycoproteins are postulated to have an immunomodulatory role in protecting the fetal allograft, as well as a role in promoting maternal angiogenesis to support the fetus. Lower levels of pregnancy-specific glycoproteins have been associated with IUGR, fetal hypoxia, and increased risk for abortion, thus providing a link to the CR-associated IUGR phenotype (58,59). Among the 21 apolipoproteins sequenced, eight were upregulated in the CR condition, with the remaining 13 expressed equally in both conditions (enrichment test: P value Ͻ 0.0001).…”

Section: Resultsmentioning

confidence: 99%

Intrauterine calorie restriction affects placental DNA methylation and gene expression

Chen

Ganguly

Rubbi

et al. 2013

Physiological Genomics

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Section: Resultsmentioning

confidence: 99%

Intrauterine calorie restriction affects placental DNA methylation and gene expression

Chen

Ganguly

Rubbi

et al. 2013

Physiological Genomics

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“…PSG1a belongs to the family of PSG that are mainly synthesized by the placenta and represent early biochemical markers of syncitiotrophoblast formation. 81 It has been reported that PSG1a can turn macrophages tolerogenic and increase their ability to produce IL-10 and TGFbeta. 82,83 PSGs and particularly PSG-1a can inhibit T-cell proliferation but not directly, they rather do this via macrophages (reviewed in Martinez).…”

Section: Modulators Of the Immune Responses During Pregnancymentioning

confidence: 99%

Adaptive Immune Responses During Pregnancy

Zenclussen

2013

American J Rep Immunol

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It has long been believed that there is no immune interaction between mother and conceptus during pregnancy. This concept changed after evidence was provided that the maternal immune system is aware of the semiallogeneic conceptus and develops strategies to tolerate it. Since then, finely regulated mechanisms of active tolerance toward the fetus have been described. This Special Issue of the American Journal of Reproductive Immunology deals with these mechanisms. It begins with the description of minor histocompatibility antigens in the placenta; it further goes through adaptive immune responses toward paternal fetal antigens, mostly concentrating on regulatory T cells and molecules modulating the Th1/Th2 balance. The participation of antibody‐producing B cells in normal and pathological pregnancies is also discussed. This introductory chapter resumes the concepts presented throughout the Issue and discusses the clinical applications raised from these concepts.

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“…For dose-response experiments, mated IL-10 Ϫ/Ϫ and IL-10 ϩ/ϩ females showing overt evidence of pregnancy were administered 0.25, 2.5, or 25 g of LPS (Salmonella typhimurium; Sigma-Aldrich) in 200 l of PBS i.p. at 1100 h on gestation day (gd) 17.…”

Section: Treatment Protocolsmentioning

confidence: 99%

Essential Role for IL-10 in Resistance to Lipopolysaccharide-Induced Preterm Labor in Mice

Robertson

Skinner

Care

2006

The Journal of Immunology

175

139

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IL-10 is highly expressed in the uterus and placenta and is implicated in controlling inflammation-induced pathologies of pregnancy. To investigate the role of IL-10 in regulating preterm labor, the response of IL-10 null mutant mice to low-dose LPS in late gestation was evaluated. When IL-10 null mutant C57BL/6 (IL-10−/−) and control (IL-10+/+) mice were administered LPS on day 17 of pregnancy, the dose of LPS required to elicit 50% preterm fetal loss was 10-fold lower in IL-10−/− mice than in IL-10+/+ mice. Surviving fetuses in IL-10−/− mice exhibited fetal growth restriction at lower doses of LPS than IL-10+/+ mice. Marked elevation of LPS-induced immunoactive TNF-α and IL-6 was evident in the serum, uterus, and placenta of IL-10−/− mice, and TNF-α and IL-6 mRNA expression was elevated in the uterus and placenta, but not the fetus. Serum IL-1α, IFN-γ, and IL-12p40 were increased and soluble TNFRII was diminished in the absence of IL-10, with these changes also reflected in the gestational tissues. Administration of rIL-10 to IL-10−/− mice attenuated proinflammatory cytokine synthesis and alleviated their increased susceptibility to preterm loss. Exogenous IL-10 also protected IL-10+/+ mice from fetal loss. These data show that IL-10 modulates resistance to inflammatory stimuli by down-regulating proinflammatory cytokines in the uterus and placenta. Abundance of endogenous IL-10 in gestational tissues is therefore identified as a critical determinant of resistance to preterm labor, and IL-10 may provide a useful therapeutic agent in this common condition.

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Pregnancy specific glycoprotein 18 induces IL-10 expression in murine macrophages

Cited by 62 publications

References 29 publications

Intrauterine calorie restriction affects placental DNA methylation and gene expression

Intrauterine calorie restriction affects placental DNA methylation and gene expression

Adaptive Immune Responses During Pregnancy

Essential Role for IL-10 in Resistance to Lipopolysaccharide-Induced Preterm Labor in Mice

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