Evidence map›Paper›PMID 27465226›Full record

ReviewSeminars in immunopathology2016

Antenatal endogenous and exogenous glucocorticoids and their impact on immune ontogeny and long-term immunity.

María Emilia Solano, Megan C Holmes, Paul R Mittelstadt, Karen E Chapman, Eva Tolosa

Open access · greenAbstract readReview
PubMed Publisher
In one paragraph

Review in Seminars in immunopathology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 37 papers.

0numbers the graph read from it
0cells of the map it votes in
37citing papers in PubMed
12.4field-weighted citation impact, top 2% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

37 citing papers in PubMed, 62 citations in OpenAlex.

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  20. Risk Factors from Pregnancy to Adulthood in Multiple Sclerosis Outcome.International journal of molecular sciences · 2022
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4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

5 authors at 3 institutions in 3 countries.

María Emilia SolanoDepartment of Obstetrics and Prenatal Medicine, University Medical Center Hamburg-Eppendorf, Hamburg, Germany. e.solano@uke.de.ORCID 0000-0002-5631-9497
Megan C HolmesUniversity/BHF Centre for Cardiovascular Science, University of Edinburgh, Queen's Medical Research Institute, Edinburgh, EH16 4TJ, UK.
Paul R MittelstadtLaboratory of Immune Regulation, National Cancer Institute, National Institutes of Health, Bethesda, MD, USA.
Karen E ChapmanUniversity/BHF Centre for Cardiovascular Science, University of Edinburgh, Queen's Medical Research Institute, Edinburgh, EH16 4TJ, UK.
Eva TolosaDepartment of Immunology, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
The Queen's Medical Research Institute · GBUniversität Hamburg · DENational Institutes of Health · US

Funding

British Heart FoundationMedical Research Council MR/P002811/1Wellcome Trust
6 · The paper itself

Abstract

Endogenous levels of glucocorticoids rise during pregnancy to warrant development and maturation of the fetal organs close to birth. However, during most of the gestation, the fetus is protected from excessive biologically active endogenous glucocorticoids by placental and fetal expression of 11β-hydroxysteroid dehydrogenase 2 (11β-HSD2). Maternal stress, which may overwhelm placental 11β-HSD2 activity with high glucocorticoid levels, or administration of synthetic glucocorticoids to improve the survival chances of the premature newborn, are associated to postnatal increased risk for immune diseases. Fetal exposure to excessive glucocorticoids may underlie this altered postnatal immunity. Here, we revise the role that placental and fetal 11β-HSD2, fetal glucocorticoid exposure, and programming of the offspring's the hypothalamic-pituitary-adrenal (HPA) axis play on concerted steps in immune fetal development. We could identify gaps in knowledge about glucocorticoid-induced programming of immune diseases. Finally, based on current evidence about glucocorticoid and HPA axis-mediated immune regulation, we hypothesize on mechanisms that could drive the enhanced risk for atopies, infections, and type I diabetes in offspring that were prenatally exposed to glucocorticoids.

Indexed as

11-beta-Hydroxysteroid DehydrogenasesFemaleFetusGene Expression RegulationGlucocorticoidsHumansHypothalamo-Hypophyseal SystemImmune SystemImmunityPituitary-Adrenal SystemPlacentaPregnancyPrenatal CarePrenatal Exposure Delayed EffectsReproductive Physiological Phenomena11-beta-Hydroxysteroid DehydrogenasesGlucocorticoidsGlucocorticoidsImmune ontogenyProgramming of chronic immune diseases

Identifiers

PMID27465226
OpenAlexW2479229036

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.