Cytokines and type 1 diabetes: Role of cytokine mediated signal transduction pathways in pancreatic beta cell dysfunction

TL;DRAbstract

Type 1 diabetes is characterized by an absolute insulin deficiency resulting from the chronic and progressive destruction of pancreatic β-cells by cells of the immune system. In humans as well as animal models, pancreatic islet infiltration by macrophages and lymphocytes, insulitis, precedes β-cell destruction and overt disease development. The final cytotoxic events mediating β-cell destruction in type 1 diabetes may involve a variety of immune/inflammatory cells and products of these activated cells. Correlation studies between cytokines expressed in islets and autoinimune diabetes development in animal models suggest β-cell destruction is associated with increased TH1 and pro-inflammatory cytokines. The pro-inflammatory cytokines interleukin-1β (IL-1β), tumor necrosis factor-α TNF-α and interferon-γ IFN-γ have dramatic effects on pancreatic β-cells in vitro. This study examined the contribution of sphingomyelin and MAP kinase signaling cascades in cytokine mediated β-cell dysfunctio

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