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

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

Research output: Contribution to journalArticlepeer-review


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 hypothalamicpituitary-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.
Original languageEnglish
Pages (from-to)1-25
JournalSeminars in Immunopathology
Early online date28 Jul 2016
Publication statusE-pub ahead of print - 28 Jul 2016


  • Glucocorticoids
  • Immune ontogeny
  • Programming of chronic immune diseases


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