Abstract
209.8: Subcutaneous Nanotherapy Repurposes the Immunosuppressive Mechanism of Rapamycin to Enhance Allogeneic Islet Graft Viability
Highlights
Type 1 diabetes (T1D) is an endocrine disorder that leads to pancreatic β cell destruction and requires management with lifelong exogenous insulin therapy[1]
Neither the PS vesicular nanostructure nor the polydispersity were significantly modulated by rapamycin loading as assessed by dynamic light scattering (DLS), cryogenic transmission electron micrograph and small angle x-ray scattering (SAXS) (Fig. 2a-c)
The stability of rapamycin loading was assessed in 1X phosphate buffered saline (PBS) at 4 °C, finding approximately 94% of the drug was retained over the course of 1 month (Fig. S1)
Summary
Type 1 diabetes (T1D) is an endocrine disorder that leads to pancreatic β cell destruction and requires management with lifelong exogenous insulin therapy[1]. With the advent of the Edmonton protocol, islet transplantation has emerged as a promising treatment for T1D by eliminating the need for exogenous insulin[1]. This protocol involves three key components: acquisition of viable insulin-producing cells, surgical transplantation of these cells into a suitable physiological location to maintain glucose sensitivity and responsiveness, and an immunosuppressive regimen to maintain islet viability and protection from the host immune system[1]. While all three components remain active areas of research, the need for immunosuppression remains the key limitation preventing islet transplantation from becoming the clinical standard of care for all T1D patients[1,2]. More effective than prior immunosuppressive protocols involving intravenous steroid administration, patients undergoing transplantation procedures are still plagued by frequent graft rejection and an unpleasant array of side effects[3,4]
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