Innate Immunity in the Recognition of β-Cell Antigens in Type 1 Diabetes

Abstract

Diabetes is a chronic disease caused by the inability to produce enough insulin by the pancreatic ┚ cells or inappropriately use insulin by the peripheral tissues, and therefore, patients with diabetes are unable to control blood glucose to a normal level. Along with the industrialization and economic development, diabetes has gradually become a global health challenge as manifested by that it affects 5-10% of the world population (Home, 2003). For example, in United States alone, approximately 21 million children and adults (around 7% of the total population) have diabetes. Despite the significant advances in the development of therapeutic approaches for this devastating disease, the long-term outcome of diabetes, however, remains unsatisfied, as many complications could occur during the process of diabetes. Transient improper control of blood glucose level will result in the dangerous short-term complications such as diabetic ketoacidosis, nonketotic hyperosmolar coma, and hypoglycemia., while the life threading condition is the development of various long-term complications such as cardiovascular disease, nerve damage, chronic renal failure, retinal damage, and poor wound healing (Zhong et al., 2011). Given the fact that the administrated exogenous insulin cannot regulate glucose levels as accurately as the endogenous insulin released by the functioning pancreatic islets, diabetic patients are highly prone to the development of those complications. For example, patients with diabetes are 17 times more prone to kidney diseases (World Health Organization (WHO), 1994; Home, 2003), and diabetes also has become the most common cause of blindness in developed countries as manifested by that nearly half of the diabetic patients developed retinopathy (Amos et al., 1997). There are two types of diabetes, type1 and type 2. Type 1 diabetes (T1D), also called Insulin Dependent Diabetes Mellitus (IDDM) or juvenile diabetes, which is characterized by the selective destruction of the insulin-secreting pancreatic ┚ cells by the autoreactive immune cells. Therefore, T1D is characterized by the absolute deficiency of insulin, and patients require injection of exogenous insulin for survival, which renders the blood glucose unable