Prenatal Betamethasone interferes with immune system development and alters target cells in autoimmune diabetes.

ABSTRACT: Non-genetic factors are crucial in the pathogenesis of type 1 diabetes (T1D), a disease caused by autoimmunity against insulin-producing β-cells. Exposure to medications in the prenatal period may influence the immune system maturation, thus altering self-tolerance. Prenatal administration of betamethasone -a synthetic glucocorticoid given to women at risk of preterm delivery- may affect the development of T1D. It has been previously demonstrated that prenatal betamethasone administration protects offspring from T1D development in nonobese diabetic (NOD) mice. The direct effect of betamethasone on the immature and mature immune system of NOD mice and on target β-cells is analysed in this paper. In vitro, betamethasone decreased lymphocyte viability and induced maturation-resistant dendriti

SUBMITTER: Perna-Barrull D 

PROVIDER: S-EPMC6362293 | biostudies-literature | 2019 Feb

REPOSITORIES: biostudies-literature