Table 2.
MSCs as cell therapy to promote engraftment of transplanted islets for the treatment of type 1 diabetes.
Cell Source | Route/site of administration | Therapeutic outcome |
---|---|---|
Allogeneic bone marrow MSCs | Intraportal co-transplantation followed by IV infusions | Increased numbers of regulatory T-cells resulted in reversal of rejection episodes and prolongation of islet function.51 |
Allogeneic bone marrow MSCs | Intraportal co-transplantation | Improvement of islet graft morphology and graft revascularization. Transdifferentiation of MSCs to endothelial cells promoted revascularization.52 |
Allogeneic bone marrow MSCs | Renal capsule transplantation | Secretion of VEGE and growth factors promoted islet vasculatization and improved glycemic control.53 |
Autologous bone marrow MSCS | Omental pouch transplantation | Autologous MSCs improved graft survival through combination of grouth factors and increase of IL-10 secreting CD4+ T cells.52 |
Syngeneic and Allogeneic MSCs | Intraportal /systemic administration | Prolonged graft survival and reduced rejection of islet mass.55 |
Umbilical cord MSCs | Intra portal administration of differentiated pancreatic cells from umbilical cord MSC | Reduced blood sugar level by transdifferentiation of MSCs into insulin producing cells.56 |
Cocultue of mice islet with human cord blood MSCs | Renal capsule transplantation | Culturing of islet with MSCs promoted islet islet viability and insulin secretory function.58 |
Autologous MSCs | Renal capsule transplantation | Improved glycemic control by blocking CD25 T cell activation and IL-2 signaling.59 |