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

摘要: 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 prenatal period may influence immune system maturation, thus altering self-tolerance. Prenatal administration betamethasone -a synthetic glucocorticoid given women at risk preterm delivery- affect development T1D. It has been previously demonstrated that protects offspring from T1D nonobese diabetic (NOD) mice. The direct effect on immature and mature NOD mice target β-cells is analysed this paper. In vitro, decreased lymphocyte viability induced maturation-resistant dendritic cells, which turn impaired γδ T cell proliferation IL-17 production. exposure thymus hypotrophy newborn as well alterations cells subsets. Furthermore, β-cell growth, reduced C-peptide secretion altered expression genes related autoimmunity, metabolism islet mass tissue. These results support protection betamethasone-treated demonstrate drug alters developing Understanding how generates self-tolerance could have potential clinical relevance