Beta cell antigens

Abstract

Insulin-dependent (type 1) diabetes mellitus (IDDM) is classified as an autoimmune disorder, since it is associated with specific autoimmunity towards the insulin-producing cells in the islets of Langerhans. The disease process that results in IDDM is not fully understood and whether it is initiated by endogenous or exogenous antigens, or a combination, remains to be clarified. The clinical onset of IDDM is characterized by weight loss and an abrupt or gradual onset of hyperglycaemia; dependence on insulin injections to sustain life; presence of different types of islet cell autoantibodies in more than 90% of patients, although this is not possible to document in the individual patient and lymphocytic infiltration of the islets of Langerhans (insulitis) in about 60% of patients [1,2]. While mononuclear cell infiltration of the pancreatic islets was described in the last century, it was not until 1965 that a systematic study [1] documented the presence of insulinitis in patients with IDDM of short duration. Later it was demonstrated that the β cells were specifically eradicated [3]. Subsequent observations that organ-specific autoimmune diseases are more common among patients with IDDM [4]–6] and that IDDM was associated with certain HLA types [7,8] further supported the notion of IDDM as an autoimmune disorder. The demonstration of islet cell antibodies (ICA) using an indirect immunofluorescence test on frozen sections of human blood group pancreas [9,10] was additional evidence of islet autoimmunity.