Abstract
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.
Highlights
Specialty section: This article was submitted to Diabetes: Molecular Mechanisms, a section of the journal Frontiers in Endocrinology
We focus on the ability of betamethasone to induce alterations in the immune system, impairing the recognition of autoantigens
Betamethasone is a poor substrate for the glucocorticoid inactivating enzyme 11beta-hydroxysteroid-dehydrogenase 2 (11βHSD2), its bioactivity in the foetus lasts for several days [12] and it is known to exert long-lasting effects on the hypothalamic-pituitary-adrenal (HPA) axis and cognition in children [13, 14]
Summary
Specialty section: This article was submitted to Diabetes: Molecular Mechanisms, a section of the journal Frontiers in Endocrinology. In newborn children with low weight at birth, prenatal betamethasone administration induced a transient immunomodulatory effect in monocytes, causing diminished IL-6 and IL-10 release and downregulation of human leukocyte antigen DR (HLA-DR) expression [37].
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
