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BACKGROUND: Preclinical stages of type 1 diabetes are characterized by infiltrating T cells and by the peri- and intra-islet accumulation of pro-inflammatory mediators, such as IFNgamma. METHODS/RESULTS: Using quantitative PCR we demonstrated that mRNA specific for the IFNgamma-inducing cytokine IL-18 is upregulated in NIT-1 beta cells and intact mouse islets upon exposure to IL-1beta, IFNgamma and TNFalpha. The biological activity of IL-18 was blocked using caspase inhibitors and anti-IL-18 antibodies. Increased IL-18 expression was also detected in islets during advanced stages of insulitis and correlated with elevated transcripts for IFNgamma and for the IL-18 receptor. CONCLUSION: Thus, beta cells produce bioactive IL-18 in the course of insulitis and actively contribute to the exacerbation of inflammation leading to their own demise.

Original publication




Journal article


Horm Res

Publication Date





94 - 104


Animals, Base Sequence, Cell Line, DNA Primers, Disease Progression, Gene Expression Regulation, Interleukin-18, Islets of Langerhans, Mice, Mice, Inbred NOD, Mice, Inbred Strains, Pancreatic Diseases, Polymerase Chain Reaction, RNA, Messenger, Reverse Transcriptase Polymerase Chain Reaction, Transcription, Genetic