The Role of Pregnancy‐Specific Glycoprotein 1a (<scp>PSG</scp>1a) in Regulating the Innate and Adaptive Immune Response

Martínez, Fernando F.; Cervi, Laura; Knubel, Carolina Paola; Panzetta-Dutari, Graciela M.; Motrán, Claudia Cristina

doi:10.1111/aji.12089

Cited by 35 publications

(28 citation statements)

References 123 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The 111 up-regulated genes included multiple transcripts involved in immune activation ( CXCL14, CCL13, IL2B , SPP1 , STAT4, TNFRSF21 , TNFSF10 ), prostaglandin synthesis ( PTGES, PTGDS ), and tissue remodeling ( COL1A1 , COL1A2 , COL5A1 COL5A2 , KRT6A, KRT6C, KRT24, KRT7). Prominent among the 233 transcripts down-regulated with disadvantage were pregnancy-specific glycoproteins ( PSG5 , PSG7 , PSG11 ) and the chorionic gonadotropin beta/luteinizing hormone beta gene cluster ( CGB , CGB1 , CGB5 , CGB7 , CGB8, LGB ), which all have roles in fetal immune tolerance (Martinez et al 2013; Bansal et al 2012). Other down-regulated transcripts included suppressors of cytokine signaling ( SOCS2, A2M, PIK3AP1 ), and inhibitors of histamine and prostaglandin activity ( PGT , ABP1 ), as well as mediators of fetal nutrient access, blood supply, and organ maturation ( CGB , CGB1 , CGB5 , CGB8 , MMP12 ), and transcripts found to be hypermethylated in association with nutrient deficiency ( MEG3 , PEG10, SLC38A2 , and LEP ) (Tobi et al 2015).…”

Section: Study 1 Resultsmentioning

confidence: 99%

Maternal socioeconomic disadvantage is associated with transcriptional indications of greater immune activation and slower tissue maturation in placental biopsies and newborn cord blood

Miller

Borders

Crockett

et al. 2017

Brain, Behavior, and Immunity

View full text Add to dashboard Cite

Children from economically disadvantaged families experience worse cognitive, psychiatric, and medical outcomes compared to more affluent youth. Preclinical models suggest some of the adverse influence of disadvantage could be transmitted during gestation via maternal immune activation, but this hypothesis has not been tested in humans. It also remains unclear whether prenatal interventions can mitigate such effects. To fill these gaps, we conducted two studies. Study 1 characterized the socioeconomic conditions of 79 women during pregnancy. At delivery, placenta biopsies and umbilical blood were collected for transcriptional profiling. Maternal disadvantage was associated with a transcriptional profile indicative of higher immune activation and slower fetal maturation, particularly in pathways related to brain, heart, and immune development. Cord blood cells of disadvantaged newborns also showed indications of immaturity, as reflected in down-regulation of pathways that coordinate myeloid cell development. These associations were independent of fetal sex, and characteristics of mothers (age, race, adiposity, diabetes, pre-eclampsia) and babies (delivery method, gestational age). Study 2 performed the same transcriptional analyses in specimens from 20 women participating in CenteringPregnancy, a group-based psychosocial intervention, and 20 women in traditional prenatal care. In both placenta biopsies and cord blood, women in CenteringPregnancy showed up-regulation of transcripts found in Study 1 to be most down-regulated in conjunction with disadvantage. Collectively, these results suggest socioeconomic disparities in placental biology are evident at birth, and provide clues about the mechanistic origins of health disparities. They also suggest the possibility that psychosocial interventions could have mitigating influences.

show abstract

Section: Study 1 Resultsmentioning

confidence: 99%

Maternal socioeconomic disadvantage is associated with transcriptional indications of greater immune activation and slower tissue maturation in placental biopsies and newborn cord blood

Miller

Borders

Crockett

et al. 2017

Brain, Behavior, and Immunity

View full text Add to dashboard Cite

show abstract

“…In addition, interesting proteins such as Ficolin 3 and pregnancy-specific beta-1-glycoprotein 4 participated in innate immunity were firstly identified down-regulated in GDM plasma. Human pregnancy-specific beta-1-glycoproteins (PSGs), a representative member of the main glycoprotein family secreted by placental trophoblast, may modulate the activation of antigen-presenting cells promoting the T-cell shift of the maternal cell immunity toward a less harmful phenotype [36]. Previous studies have reported abnormal levels of PSGs in complicated pregnancies and have shown their importance for the maintenance of a successful pregnancy [37].…”

Section: Discussionmentioning

confidence: 99%

Early second-trimester plasma protein profiling using multiplexed isobaric tandem mass tag (TMT) labeling predicts gestational diabetes mellitus

Zhao

Wang

et al. 2015

Acta Diabetol

View full text Add to dashboard Cite

show abstract

“…The actions of PSG1 on cells of the innate and adaptive immune system have been recently reviewed in (Martinez et al, 2013). IL-10 and TGF-b are suppressor cytokines, which are interrelated (Kitani et al, 2003, Li et al, 2006, Moore et al, 2001.…”

Section: Pregnancy-specific Glycoproteins 277mentioning

confidence: 99%

Pregnancy-specific glycoproteins: complex gene families regulating maternal-fetal interactions

2014

View full text Add to dashboard Cite

The pregnancy-specific glycoproteins (PSGs) are the most abundant trophoblastic proteins in maternal blood during human pregnancy and they appear to be exclusive to species with hemochorial placentation. There are ten protein-coding human PSG genes (PSG1 -PSG9, PSG11) and also multiple PSG genes in non-human primates, rodents and bats. Several studies indicate that PSGs have immunoregulatory, pro-angiogenic, and anti-platelet functions. Some PSGs have been shown to bind different moieties on the surface of cells, including the tetraspanin CD9, heparan sulphate, and specific integrins. Recently, PSG1 was shown to associate with and activate the anti-inflammatory cytokines transforming growth factor (TGF)-b1 and TGF-b2 making PSG1 one of the few known biological activators of these important cytokines. TGF-bs regulate many biological processes essential for pregnancy success including trophoblast invasion and proliferation, angiogenesis, extracellular matrix formation and tolerance to the fetal semi-allograft. As summarized in this review, progress has been made in recent years towards a better understanding of the functions of these proteins which were originally described in the early 1970s, but more research will likely contribute to demonstrate their importance for a successful pregnancy.

show abstract

The Role of Pregnancy‐Specific Glycoprotein 1a (PSG1a) in Regulating the Innate and Adaptive Immune Response

Abstract: CitationMartinez FF, Cervi L, Knubel CP, PanzettaDutari GM, Motran CC. The role of pregnancyspecific glycoprotein 1a (PSG1a) in regulating the innate and adaptive immune response.

Cited by 35 publications

References 123 publications

Maternal socioeconomic disadvantage is associated with transcriptional indications of greater immune activation and slower tissue maturation in placental biopsies and newborn cord blood

Maternal socioeconomic disadvantage is associated with transcriptional indications of greater immune activation and slower tissue maturation in placental biopsies and newborn cord blood

Early second-trimester plasma protein profiling using multiplexed isobaric tandem mass tag (TMT) labeling predicts gestational diabetes mellitus

Pregnancy-specific glycoproteins: complex gene families regulating maternal-fetal interactions

Contact Info

Product

Resources

About