Lipopolysaccharide-induced cytokine signaling activates a temporal innate defense program and represses pancreatic β-cell identity.

ABSTRACT: Cytokine exposure has been promoted as one cause for the loss of β-cell mass during the development of type 1 diabetes. While in vitro studies have shown that cytokines inhibit insulin secretion and induce islet degeneration, interventions targeting these soluble mediators have had limited success in preventing disease development in rodents and humans. To understand the in vivo actions of cytokines in the endocrine pancreas, we explored the transcriptional responses of islets to endogenously produced cytokines following immune stimulation with the bacterial pathogen-associated molecular pattern lipopolysaccharide. We found that endogenous cytokine production in response to lipopolysaccharide administration stimulates the rapid, time-dependent expression of antiviral, antibacterial, and an

SUBMITTER: Bartosiak JT 

PROVIDER: S-EPMC12663513 | biostudies-literature | 2025 Oct

REPOSITORIES: biostudies-literature