Immunology in the Clinic Review Series; focus on metabolic diseases: development of islet autoimmune disease in type 2 diabetes patients: potential sequelae of chronic inflammation

Abstract

Historically, the development of type 2 diabetes has been considered not to have an autoimmune component, in contrast to the autoimmune pathogenesis of type 1 diabetes. In this review we will discuss the accumulating data supporting the concept that islet autoreactivity and inflammation is present in type 2 diabetes pathogenesis, and the islet autoimmunity appears to be one of the factors associated with the progressive nature of the type 2 diabetes disease process.

Fig. 1

Fasting and glucagon-stimulated C-peptide in phenotypic type 2 diabetes patients separated by antibody-negative (n = 17) and antibody-positive (n = 19) independent of T cell reactivity (a) or separated by T cell responses to islet proteins irrespective of autoantibody responses (b). T cell^– (n = 13) and T cell⁺ (n = 23). Horizontal bars represent means [53].

Fig. 2

Similarities and differences identified in islet proteins recognized by peripheral blood mononuclear cells from type 1 diabetes and autoantibody-positive phenotypic type 2 diabetes patients. Asterisks identify significant (P < 0·05) differences in percentage of patients responding to a particular molecular weight region containing islet proteins [66].