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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

doi: 10.1073/pnas.052706899

Frontiers in Pharmacology, 12, 692015

Travma Acil Cerrahi Derg