How inflammation contributes to Type 2 diabetes development is described in an online report this week in Nature Immunology.
Type 2 diabetes (T2D) is a common life-threatening condition characterized by the deposition of amyloid protein fibrils in the pancreas. The significance of amyloid protein to the development of diabetes was unclear until now.
Seth Masters and colleagues show that macrophages — an immune cell associated with clearance of cellular debris — ingest these amyloid fibrils. This switches on so-called “angry macrophages” causing them to secrete a number of inflammatory proteins that induce destruction of insulin-secreting cells and lead to T2D development.
This work therefore suggests that strategies that can prevent activation of pancreatic macrophages by amyloid fibrils may prove useful in the treatment and prevention of T2D.
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