ArticleFrontiers in immunology2017
Prenatal Administration of Betamethasone Causes Changes in the T Cell Receptor Repertoire Influencing Development of Autoimmunity.
Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 16 citations in OpenAlex.
- Pharmacokinetics and Pharmacodynamics of Intramuscular and Oral Betamethasone and Dexamethasone in Reproductive Age Women in India.Clinical and translational science · 2020Trial
- Impact of Betamethasone Pretreatment on Engrafment of Cord Blood-Derived Hematopoietic Stem Cells.Archivum immunologiae et therapiae experimentalis · 2022Article
- Impact of Glucocorticoids on Cardiovascular System-The Yin Yang Effect.Journal of personalized medicine · 2022Review
- Prenatal Betamethasone Exposure and its Impact on Pediatric Type 1 Diabetes Mellitus: A Preliminary Study in a Spanish Cohort.Journal of diabetes research · 2022Article
- Premature birth carries a higher risk of nephrotic syndrome: a cohort study.Scientific reports · 2021Article
- Glucocorticoids in T cell development, differentiation and function.Nature reviews. Immunology · 2021Review
- Article
- Immune System Remodelling by Prenatal Betamethasone: Effects on β-Cells and Type 1 Diabetes.Frontiers in endocrinology · 2020Review
- Prenatal Betamethasone interferes with immune system development and alters target cells in autoimmune diabetes.Scientific reports · 2019Article
- Progesterone modulates the T-cell response via glucocorticoid receptor-dependent pathways.American journal of reproductive immunology (New York, N.Y. : 1989) · 2019Article
- Interactions Between the Neuroendocrine System and T Lymphocytes in Diabetes.Frontiers in endocrinology · 2018Review
Corrections and comments
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Authors and funding
13 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Prenatal glucocorticoids are routinely administered to pregnant women at risk of preterm delivery in order to improve survival of the newborn. However, in half of the cases, birth occurs outside the beneficial period for lung development. Glucocorticoids are potent immune modulators and cause apoptotic death of immature T cells, and we have previously shown that prenatal betamethasone treatment at doses eliciting lung maturation induce profound thymocyte apoptosis in the offspring. Here, we asked if there are long-term consequences on the offspring's immunity after this treatment. In the non-obese diabetic mouse model, prenatal betamethasone clearly decreased the frequency of pathogenic T cells and the incidence of type 1 diabetes (T1D). In contrast, in the lupus-prone MRL/lpr strain, prenatal glucocorticoids induced changes in the T cell repertoire that resulted in more autoreactive cells. Even though glucocorticoids transiently enhanced regulatory T cell (Treg) development, these cells did not have a protective effect in a model for multiple sclerosis which relies on a limited repertoire of pathogenic T cells for disease induction that were not affected by prenatal betamethasone. We conclude that prenatal steroid treatment, by inducing changes in the T cell receptor repertoire, has unforeseeable consequences on development of autoimmune disease. Our data should encourage further research to fully understand the consequences of this widely used treatment.
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