Abstract
Pancreatic islet transplantation as a therapeutic option for type 1 diabetes mellitus is gaining widespread attention because this approach can restore physiological insulin secretion, minimize the risk of hypoglycemic unawareness, and reduce the risk of death due to severe hypoglycemia. However, there are many obstacles contributing to the early mass loss of the islets and progressive islet loss in the late stages of clinical islet transplantation, including hypoxia injury, instant blood-mediated inflammatory reactions, inflammatory cytokines, immune rejection, metabolic exhaustion, and immunosuppression-related toxicity that is detrimental to the islet allograft. Here, we discuss the fate of intrahepatic islets infused through the portal vein and propose potential interventions to promote islet allograft survival and improve long-term graft function.
Highlights
Insulin deficiency caused by autoimmune injury of islet β cells is the primary cause of type 1 diabetes mellitus (T1DM)
Over the past 20 years, significant progress has been made in the management of islet cells and the outcome of clinical islet transplantation
We focused on the fate of the islets infused through the portal vein, which are subjected to multiple insults, including anoxia/ischemiareperfusion injury, instant blood-mediated inflammatory reaction (IBMIR), potent autoimmune and alloimmune rejections, metabolic exhaustion, and immunosuppression-related toxicity (Figure 1)
Summary
Insulin deficiency caused by autoimmune injury of islet β cells is the primary cause of type 1 diabetes mellitus (T1DM). Over the past 20 years, significant progress has been made in the management of islet cells and the outcome of clinical islet transplantation. In some leading islet transplant centers, it is possible to achieve 5-year insulin independence rates of 50–70%, on a par with whole-pancreas transplantation in T1DM patients [1,2,3,4,5]. Many challenges remain in clinical islet transplantation. We focused on the fate of the islets infused through the portal vein, which are subjected to multiple insults, including anoxia/ischemiareperfusion injury, instant blood-mediated inflammatory reaction (IBMIR), potent autoimmune and alloimmune rejections, metabolic exhaustion, and immunosuppression-related toxicity (Figure 1). We propose protective strategies to circumvent these adverse events to alleviate the loss of islets and improve the long-term outcomes of transplantation
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