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JDRF is committed to accelerating the development of a beta cell replacement therapy with a replenishable source of insulin-producing cells capable of reversing hypoglycemia unawareness, restoring glucose control, and improving the management of insulin treatment in type 1 diabetes (T1D) without chronic systemic immunosuppression. To accomplish this goal, JDRF invites applications to define encapsulation systems and advance preclinical or clinical proof of concept studies aimed at validating beta cell replacement approaches for individuals living with T1D.
Transplantation of pancreatic islets is a proven treatment capable of restoring glucose control in individuals with severe life threatening hypoglycemia unawareness. However, the application of islet transplantation is limited due to the requirement for lifelong immunosuppression therapy and a shortage of islets from donor pancreata. One of the goals of the Beta Cell Replacement program at JDRF is to develop safe therapies that pair insulin-producing cells with supportive and protective strategies capable of restoring long-term beta cell function without the need for chronic immunosuppression. Currently, encapsulated systems consisting of a protective barrier enclosing a cell product derived from porcine sources or human pluripotent stem cells are considered the most likely candidates to have nearer term clinical impact. For the last five years, research teams funded by JDRF and often brought together through a Consortium, have made significant progress in the field of encapsulation by advancing the development of bioengineered materials, optimizing human stem cells and porcine islets as a cell source for therapy, and providing preclinical proof-of-concept for several encapsulated systems. However, key challenges remain to be addressed when considering replacement therapies with encapsulation systems. These include the recognition of materials leading to a foreign body/fibrotic response, oxygenation and diffusion of nutrients including glucose/insulin through the membranes to prevent hypoxia and malnourishment, glucose sensing and insulin release kinetics, and the lack of an optimal microenvironment at the implantation site to allow long-term cell viability and function.