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Virus-like infection induces human ? cell dedifferentiation #MMPMID29415896
Oshima M; Knoch KP; Diedisheim M; Petzold A; Cattan P; Bugliani M; Marchetti P; Choudhary P; Huang GC; Bornstein SR; Solimena M; Albagli-Curiel O; Scharfmann R
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Type 1 diabetes (T1D) is a chronic disease characterized by an autoimmune-mediated destruction of insulin-producing pancreatic ? cells. Environmental factors such as viruses play an important role in the onset of T1D and interact with predisposing genes. Recent data suggest that viral infection of human islets leads to a decrease in insulin production rather than ? cell death, suggesting loss of ? cell identity. We undertook this study to examine whether viral infection could induce human ? cell dedifferentiation. Using the functional human ? cell line EndoC-?H1, we demonstrate that polyinosinic-polycytidylic acid (PolyI:C), a synthetic double-stranded RNA that mimics a byproduct of viral replication, induces a decrease in ? cell?specific gene expression. In parallel with this loss, the expression of progenitor-like genes such as SOX9 was activated following PolyI:C treatment or enteroviral infection. SOX9 was induced by the NF-?B pathway and also in a paracrine non?cell-autonomous fashion through the secretion of IFN-?. Lastly, we identified SOX9 targets in human ? cells as potentially new markers of dedifferentiation in T1D. These findings reveal that inflammatory signaling has clear implications in human ? cell dedifferentiation.
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