title: Epitope analysis of GAD65 autoantibodies in Japanese patients with autoimmune diabetes.
abstract: Type 1 diabetes is an organ-specific autoimmune disease characterized by T cell-mediated destruction of pancreatic beta cells. In Japanese population, the incidence of type 1 diabetes in children is very low compared to European countries. However, there are more patients with type 1 diabetes in adults, including latent autoimmune diabetes in adults (LADA). The circulating autoantibodies to multiple islet autoantigens including GAD, insulin, and IA-2 are the important immunological features of type 1 diabetes. The prevalences of anti-islet autoantibodies in patients with Japanese type 1 diabetes are 60-70% for GAD autoantibodies, 45-50% for insulin autoantibodies (IAA), and 60-65% for IA-2 autoantibodies at disease onset, which are similar to those reported in Caucasian patients. With combinatorial analysis of these autoantibodies, 90% of patients express at least one of these autoantibodies and are classified as type 1A diabetes. Although the majority of patients with type 1 diabetes are young, lean, and ketosis-prone, there are a number of patients with type 1 diabetes initially diagnosed as having type 2 diabetes at disease onset called LADA. These patients with LADA often progress toward an insulin-deficient state within several years after diagnosis. High levels of GAD autoantibodies have a high predictive value for future insulin deficiency in LADA. Further, epitope analysis of GAD65 autoantibodies may be helpful to predict future insulin dependency in LADA patients. In conclusion, Japanese patients with type 1 diabetes are clinically heterogeneous and the determination of immunological features are helpful to clarify the characteristics of the Japanese type 1 diabetic syndrome.
authors.affiliation: Unit of Metabolism/Diabetes and Clinical Nutrition, Nagasaki University School of Medicine, Nagasaki, Japan. eijikawa@.net.nagasaki-u.ac.jp
authors.forename: Eiji
authors.initials: E
authors.lastname: Kawasaki
authors.forename: Norio
authors.initials: N
authors.lastname: Abiru
authors.forename: Akane
authors.initials: A
authors.lastname: Ide
authors.forename: Fuyan
authors.initials: F
authors.lastname: Sun
authors.forename: Tetsuya
authors.initials: T
authors.lastname: Fukushima
authors.forename: Ryoko
authors.initials: R
authors.lastname: Takahashi
authors.forename: Hironaga
authors.initials: H
authors.lastname: Kuwahara
authors.forename: Naruhiro
authors.initials: N
authors.lastname: Fujita
authors.forename: Atsushi
authors.initials: A
authors.lastname: Kita
authors.forename: Katsuya
authors.initials: K
authors.lastname: Oshima
authors.forename: Shigeo
authors.initials: S
authors.lastname: Uotani
authors.forename: Hironori
authors.initials: H
authors.lastname: Yamasaki
authors.forename: Yoshihiko
authors.initials: Y
authors.lastname: Yamaguchi
authors.forename: Katsumi
authors.initials: K
authors.lastname: Eguchi
mesh_terms: D001323:Autoantibodies / Q000737:chemistry*; D001324:Autoantigens / Q000276:immunology; D003922:Diabetes Mellitus, Type 1 / Q000188:drug therapy / Q000276:immunology*; D000939:Epitopes / Q000276:immunology*; D005968:Glutamate Decarboxylase / Q000276:immunology*; D006801:Humans; D007328:Insulin / Q000008:administration & dosage / Q000627:therapeutic use; D007515:Islets of Langerhans / Q000276:immunology; D007527:Isoenzymes / Q000276:immunology*; D007564:Japan
chemical_list: D001323:Autoantibodies; D001324:Autoantigens; D000939:Epitopes; D007328:Insulin; D007527:Isoenzymes; D005968:Glutamate Decarboxylase; C401141:glutamate decarboxylase 2