Cytohistologic analyses of β cell dedifferentiation induced by inflammation in human islets

β cell dedifferentiation is a key mechanism for dysfunction in type 2 diabetes mellitus (T2DM). Although it has been indicated previous studies that could be induced by inflammation, the cytohistologic analyses of inflammation-induced human islets lacking. The present study aims to cytohistologically characterize treated proinflammatory cytokines Interleukin-1β/Tuman necrosis factor-α/Interferon-γ (IL-1β/TNF-α/IFN-γ), which frequently-used method mimic islet inflammation studies. loss cytosolic FOXO1 expression, nucleic NKX6.1 and gain ALDH1A3 expression cells are proclaimed as marking events dedifferentiation. Taking advantages from organ donors immunofluorescence staining methods, visualized marked different markers, quantified frequency each event well. We successfully captured described characteristics differentiating/differentiated cells. found dedifferentiated were increased islets, evidenced increase with translocated nucleus (INS + FOXO nuc ), exported cyt - dual insulin progenitor marker ALDH1A3. Consistently, we IL-1β/TNF-α/IFN-γ treatment reduced mRNA but elevated genes. This gives most direct evidence supports concept anti-inflammation treatments may facilitate alleviating T2DM islets.