Multifactorial Disease of Unknown Aetiology

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.

Type 1 diabetes (T1D) is an autoimmune disease caused by the selective destruction of insulin-producing β-cells. The trigger, however, remains unknown. Postnatal environmental determinants have been thoroughly studied as risk factors but a crucial phase for the immune system development, the late prenatal stage, has been poorly investigated. Specifically, the interaction of drugs commonly used during late pregnancy with T1D and the pancreatic β-cells remains unexplored. Nonetheless, some studies reveal the importance of the prenatal stage and the prematurity of the newborn in the development of T1D. An indirect demonstration of how critical the in utero environment is in T1D development arises from the studies in twins: heterozygotic twins have an increased concordance of T1D when compared to non-twin siblings, underlining the potential relevance of prenatal factors and their influence in the development of autoimmunity.

Regards

David Paul
Editorial Assistant
Pancreatic Disorder and Therapy