Mast cells infiltrate pancreatic islets in human type 1 diabetes

Background and aims. Beta cell destruction in human type 1 diabetes occurs through the interplay of genetic and environmental factors and is mediated by immune cell infiltration of pancreatic islets. The aim of the present study was to investigate the role of different inflammatory cells in the type 1 diabetes insulitis scenario. Materials and Methods. Pancreatic samples were obtained from the glands of 7 T1D, 7 T2D and 7 ND organ donors, with similar clinical features, and processed by standard electron microscopy techniques. Results. A greater amounts of mast cells were found to infiltrate pancreatic islets in human type 1 diabetic samples, than in control and type 2 diabetic pancreases. Evidence of mast cell degranulation was shown, and the extent of the infiltration was correlated with beta cell damage. In addition, we observed that histamine, the amine highly expressed in mast cells, could directly contribute to beta cell apoptosis by a caspase-independent pathway. Conclusion. These findings suggest that mast cells may be responsible, at least in part, of the immune-mediated beta cell alterations in human type 1 diabetes. If so, protection of beta cells in type 1 diabetes might benefit from inhibition of mast cell activation and degranulation.