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Human pancreatic beta cells are specialized endocrine cells located within the islets of Langerhans that are responsible for the synthesis, storage, and glucose-regulated release of insulin [1]. In Type 1 Diabetes, these cells are selectively destroyed by an autoimmune response, leading to a critical deficiency in insulin and the loss of systemic glucose homeostasis [3]. The therapeutic strategy of transplanting these cells—whether sourced from cadaveric donors or generated from human pluripotent stem cells (hPSCs)—aims to restore endogenous glycemic control and eliminate the need for exogenous insulin injections [2]. Unlike traditional insulin therapy, transplanted beta cells provide a dynamic, physiological response to blood glucose fluctuations, significantly reducing the risk of severe hypoglycemia [4]. However, the clinical application of this therapy is currently limited by the requirement for chronic immunosuppression to prevent alloimmune rejection and the potential for autoimmune recurrence [1]. Emerging technologies, such as cell encapsulation and the development of hypoimmune stem cell lines, are being explored to protect these cells from the host immune system without the need for systemic drugs [3].
Restoration of physiological, glucose-responsive insulin secretion to maintain systemic glycemic control and reduce glycemic variability.
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