Type 1 diabetes (T1D) is a chronic autoimmune condition characterized by islet inflammation resulting from poorly define combinations of genetic, immunologic, and environmental factors. Being an auto-immune disease, T1D evokes the infiltration of autoreactive CD8+ and CD4+ T cells in the islets which in turn induces the production of pro-inflammatory cytokines e.g., IFNa, IFN?, TNFa resulting in beta-cell death. The pathology elicits profound changes in energy metabolism and mitochondrial function in insulin-deprived conditions of the affected individuals. However, little is known about the cause and effect of changes in beta-cell energy metabolism induced by the inflammatory milieu. Understanding metabolic modulators during beta-cell pathophysiology will advance the field for more customized cellular therapy.
Although nonobese diabetic (NOD) mouse, the closest preclinical human T1D model provided invaluable information to understand the disease, the remarkable differences in tissue pathology of human T1D donor pancreas from that of the mice warrants better models to understand the beta-cell physiology. Human pluripotent stem cells (hPSCs) differentiation towards islet-like clusters (SC-islets) model provides a pre-eminent tool to understand pancreatic development and disease modeling. SC-islets model provides a better tool to understand human T1D pathophysiology, including pro-inflammatory cytokines actions, cellular communication with immune cells, and beta-cells metabolic reprogramming. Identifying extrinsic modulators of diseased beta-cells will be a valuable tool to further understand the T1D etiology and advance attempts to improve cellular therapy for T1D.
In this Research Topic, we would welcome Original Article, Mini Review, Perspective and Methods covering, but not limited to, the applications of the human SC-islets model to understand the effect of T1D associated cytokines on beta-cells function and survival; communication between immune cells and islets cells; beta-cell metabolism and the alter metabolic profile mimicking the T1D condition. We are looking forward to your submission and contribution to further understand the human T1D etiology through the eye of SC-islets model.
Type 1 diabetes (T1D) is a chronic autoimmune condition characterized by islet inflammation resulting from poorly define combinations of genetic, immunologic, and environmental factors. Being an auto-immune disease, T1D evokes the infiltration of autoreactive CD8+ and CD4+ T cells in the islets which in turn induces the production of pro-inflammatory cytokines e.g., IFNa, IFN?, TNFa resulting in beta-cell death. The pathology elicits profound changes in energy metabolism and mitochondrial function in insulin-deprived conditions of the affected individuals. However, little is known about the cause and effect of changes in beta-cell energy metabolism induced by the inflammatory milieu. Understanding metabolic modulators during beta-cell pathophysiology will advance the field for more customized cellular therapy.
Although nonobese diabetic (NOD) mouse, the closest preclinical human T1D model provided invaluable information to understand the disease, the remarkable differences in tissue pathology of human T1D donor pancreas from that of the mice warrants better models to understand the beta-cell physiology. Human pluripotent stem cells (hPSCs) differentiation towards islet-like clusters (SC-islets) model provides a pre-eminent tool to understand pancreatic development and disease modeling. SC-islets model provides a better tool to understand human T1D pathophysiology, including pro-inflammatory cytokines actions, cellular communication with immune cells, and beta-cells metabolic reprogramming. Identifying extrinsic modulators of diseased beta-cells will be a valuable tool to further understand the T1D etiology and advance attempts to improve cellular therapy for T1D.
In this Research Topic, we would welcome Original Article, Mini Review, Perspective and Methods covering, but not limited to, the applications of the human SC-islets model to understand the effect of T1D associated cytokines on beta-cells function and survival; communication between immune cells and islets cells; beta-cell metabolism and the alter metabolic profile mimicking the T1D condition. We are looking forward to your submission and contribution to further understand the human T1D etiology through the eye of SC-islets model.
