Immune System Remodelling by Prenatal Betamethasone
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Immune System Remodelling by Prenatal Betamethasone : Effects on β-Cells and Type 1 Diabetes. / Perna-Barrull, David; Gieras, Anna; Rodriguez-Fernandez, Silvia; Tolosa, Eva; Vives-Pi, Marta.
in: FRONT ENDOCRINOL, Jahrgang 11, 2020, S. 540.Publikationen: SCORING: Beitrag in Fachzeitschrift/Zeitung › SCORING: Review › Forschung
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TY - JOUR
T1 - Immune System Remodelling by Prenatal Betamethasone
T2 - Effects on β-Cells and Type 1 Diabetes
AU - Perna-Barrull, David
AU - Gieras, Anna
AU - Rodriguez-Fernandez, Silvia
AU - Tolosa, Eva
AU - Vives-Pi, Marta
N1 - Copyright © 2020 Perna-Barrull, Gieras, Rodriguez-Fernandez, Tolosa and Vives-Pi.
PY - 2020
Y1 - 2020
N2 - Type 1 diabetes (T1D) is a multifactorial disease of unknown aetiology. Studies focusing on environment-related prenatal changes, which might have an influence on the development of T1D, are still missing. Drugs, such as betamethasone, are used during this critical period without exploring possible effects later in life. Betamethasone can interact with the development and function of the two main players in T1D, the immune system and the pancreatic β-cells. Short-term or persistent changes in any of these two players may influence the initiation of the autoimmune reaction against β-cells. In this review, we focus on the ability of betamethasone to induce alterations in the immune system, impairing the recognition of autoantigens. At the same time, betamethasone affects β-cell gene expression and apoptosis rate, reducing the danger signals that will attract unwanted attention from the immune system. These effects may synergise to hinder the autoimmune attack. In this review, we compile scattered evidence to provide a better understanding of the basic relationship between betamethasone and T1D, laying the foundation for future studies on human cohorts that will help to fully grasp the role of betamethasone in the development of T1D.
AB - Type 1 diabetes (T1D) is a multifactorial disease of unknown aetiology. Studies focusing on environment-related prenatal changes, which might have an influence on the development of T1D, are still missing. Drugs, such as betamethasone, are used during this critical period without exploring possible effects later in life. Betamethasone can interact with the development and function of the two main players in T1D, the immune system and the pancreatic β-cells. Short-term or persistent changes in any of these two players may influence the initiation of the autoimmune reaction against β-cells. In this review, we focus on the ability of betamethasone to induce alterations in the immune system, impairing the recognition of autoantigens. At the same time, betamethasone affects β-cell gene expression and apoptosis rate, reducing the danger signals that will attract unwanted attention from the immune system. These effects may synergise to hinder the autoimmune attack. In this review, we compile scattered evidence to provide a better understanding of the basic relationship between betamethasone and T1D, laying the foundation for future studies on human cohorts that will help to fully grasp the role of betamethasone in the development of T1D.
U2 - 10.3389/fendo.2020.00540
DO - 10.3389/fendo.2020.00540
M3 - SCORING: Review article
C2 - 32849311
VL - 11
SP - 540
JO - FRONT ENDOCRINOL
JF - FRONT ENDOCRINOL
SN - 1664-2392
ER -