Abstract
Diabetes mellitus is a disease of antiquity with an estimated 20,000 people dying prematurely per year due to diabetes associated disease. Type 1 diabetes results from autoimmune destruction of insulin-producing pancreatic cells. Much effort has been dedicated to figure out the autoimmune background of this disease with a view to exploring how the immune system can be manipulated to prevent its occurrence. In this review, we explore the autoimmune basis of type I diabetes mellitus and equally the immune interventions that have been and are being employed to prevent type I diabetes mellitus.
Highlights
Diabetes mellitus is a chronic endocrinological disorder manifesting as high blood glucose levels either due to insufficient secretion of insulin by the pancreas or improper utilization of insulin by target cells [1]
It was concluded that the C-terminal domain of human zinc transporter Slc30A8 (ZnT8) contains at least two discrete epitopes, one of which is critically dependent upon the arginine residue at position 325 [12]
Studies of nonobese mice with diabetes show that administration of the GAD65 isoform can prevent autoimmune destruction of beta cells. These findings suggest that GAD65 administration could be used as a preventive treatment for type I diabetes (TID) [30]
Summary
Diabetes mellitus is a chronic endocrinological disorder manifesting as high blood glucose levels either due to insufficient secretion of insulin by the pancreas or improper utilization of insulin by target cells [1]. Despite recent progress in therapy and management of diabetes mellitus, diabetes remains a serious disease with life-threatening complications It is by far the most common metabolic disease [9]. An avalanche of screening programs is used to identify high-risk subjects who may benefit from an early intervention, with the ultimate goal of curtailing the development of overt type I diabetes mellitus in those at risk for the disease, using both specific and safe strategies. These emerging novel preventive and regenerative therapies are aimed at preserving β-cell mass and delay the onset of diabetes. There have been many studies designed to interdict the TID disease process, mostly by altering the immune system, both during the stage of evolution of the disease and at the time of disease onset [8]
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