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Provided that there is no accompanying inflammatory reaction, the two terms are synonymous

This suggests that the activation of insulitis, which underpins the initiation and progression of diabetes, requires the immune tolerance to -cell autoantigens to be broken ( Analyses of human insulitis lesions have suggested that signals released from stressed -cells precedes, and putatively initiates, the development of insulitis ( Beta cells rapidly respond to the minute-to-minute fluctuations in blood glucose levels by tightly regulating insulin secretion

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