Role of interleukin -1β in pancreatic islet cells dysfunction and apoptosis in pancreatic islet transplantation

The need to protect pancreatic islet beta cells from pro-inflammatory cytokines plays an indispensable role in the prevention of the pancreatic islet dysfunction. Inflammatory cytokines including 1L-1β apoptotic signaling pathway, TNF-alpha and IFN-y are implicated in, pancreatic islet B-cell dysfunction and apoptosis of islet cells after transplantation. The cytokine interleukin-1β (IL-1) is a potential mediator of B cell dysfunction and damage in conditions such as diabetes mellitus. It is believed that a deeper understanding of the mechanism in which pancreatic islets are destroyed by cytokines can be of great help in preventing diseases such as diabetes and improvement of islet transplantation. More research is needed to investigate the best way possible for blocking of interleukin- 1β induced pancreatic islets damage. Most studies suggest that circulating 1L-1β is an indispensable factor that modulates both alpha and B-cell secretory functions in vivo and that 1L-1β should be considered a contributory pathogenetic factor in the development of insulin-dependent (type 1) diabetes mellitus and other conditions that may be associated with pancreatic islet dysfunction. The goal of this review is to provide a general overview of the roles played by interleukin-1β in pancreatic islet dysfunction leading to both major forms of diabetes as well as pancreatic islet apoptosis during islet transplantation.