Type I (insulin-dependent) diabetes is a Th1-and Th2-mediated autoimmune disease

Abstract

Type I (insulin-dependent) diabetes (IDDM) is an autoimmune disease with an unknown etiology but with a definite outcome, resulting in the progressive misdirected immunologic destruction of insulin-secreting pancreatic β islet cells by autoreactive leukocytes and their mediators (3). Even though the precise cause of the disease remains unclear, a combination of genetic, immunologic, and nongenetic factors contributes to the onset and progression of IDDM (3, 52). Specific HLA antigens, in particular DR3 and DR4, have been associated with increased risk for IDDM development (52, 89), while DR2 alleles generally have been described as “protective” of IDDM (86).