Would blockage of cytokines improve the outcome of pancreatic islet transplantation?

It has been estimated that up to 60% of pancreatic islet tissue undergoes apoptosis within the first several days post-transplantation. This strongly suggests the involvement of an inflammatory event other than alloantigen-specific immune reaction following islet transplantation which contributes to partial destruction of grafts. Inflammatory cytokines including IL-1beta, TNF-alpha and IFN-gamma are implicated in the pancreatic islet beta-cell death and functional loss during autoimmune diabetes and also seem to be involved in early loss of islet mass in islet transplantation. Inflammatory cytokines and free oxygen radicals released in situ could cause apoptosis and the functional impairment of islets after islet transplantation and graft failure. It can be hypothesized that preventing destruction of transplanted islets using cytokine blockade could be helpful in improving islet transplantation outcome. Several approaches have been made based on this hypothesis to examine the effect of inflammatory blockade on the islets survival and functional islet mass. Further investigations are required to identify most efficient way for block of cytokine-induced damage in pancreatic islets transplantation.