title: Humoral immune response to islet autoantigens in Japanese patients with type 1 diabetes.
abstract: In this study, we evaluated autoantibodies to IA-2 (IA-2As), glutamic acid decarboxylase 65 (GADAs), and islet cell antibodies (ICAs) in 233 patients with type 1 diabetes (M:F = 90:143, mean duration 4.0 +/- 6.7 yr) as a cross-sectional study. Of 233 patients with type 1 diabetes, IA-2A was detected in 58% of patients with duration within 2 weeks, 61% of patients with duration <1 yr, 41% of patients with diabetes for 1-3 yr, 29% for 4-9 yr, and 21% for >or=10 yr. These prevalences were similar to those of ICA, while the prevalence of GADA was not influenced by duration of diabetes with positivity of 63-74%. Thus, as the duration of diabetes became longer, the frequency of GADA(+)/IA-2A(-) patients increased and the frequency of GADA(+)/IA-2A(+) patients decreased. However, the frequency of GADA(-)/IA-2A(+) patients was not influenced by duration of diabetes. The prevalence of IA-2A was significantly higher in abrupt-onset group (68%, n= 79) compared to the slowly progressive group (23%, n= 22) in new-onset patients (P= 0.0001). However, there was no difference in the IA-2A frequency between these two groups (abrupt-onset 26%, n= 53 vs. slowly progressive 24%, n= 21) in patients with long-standing disease, suggesting that IA-2A positivity might persist in patients with slowly progressive type 1 diabetes. These results emphasize the heterogeneity of humoral autoimmunity to protein tyrosine phosphatase-like molecules, but not to GAD, in patients with type 1 diabetes.
authors.affiliation: Department of Metabolism, Nagasaki University Hospital of Medicine and Dentistry, Nagasaki, Japan. eijikawa@nagasaki-u.ac.jp
authors.forename: Eiji
authors.initials: E
authors.lastname: Kawasaki
authors.forename: Genpei
authors.initials: G
authors.lastname: Kuriya
authors.forename: Tsuyoshi
authors.initials: T
authors.lastname: Satoh
authors.forename: Keiichiro
authors.initials: K
authors.lastname: Fujishima
authors.forename: Akie
authors.initials: A
authors.lastname: Moriuchi
authors.forename: Keiko
authors.initials: K
authors.lastname: Fukushima
authors.forename: Masako
authors.initials: M
authors.lastname: Ozaki
authors.forename: Norio
authors.initials: N
authors.lastname: Abiru
authors.forename: Hironori
authors.initials: H
authors.lastname: Yamasaki
authors.forename: Katsumi
authors.initials: K
authors.lastname: Eguchi
mesh_terms: D000293:Adolescent; D000328:Adult; D000906:Antibodies / Q000097:blood; D000917:Antibody Formation / Q000502:physiology*; D001324:Autoantigens / Q000276:immunology*; D002648:Child; D003430:Cross-Sectional Studies; D003922:Diabetes Mellitus, Type 1 / Q000097:blood / Q000453:epidemiology / Q000276:immunology*; D018450:Disease Progression; D005260:Female; D005968:Glutamate Decarboxylase / Q000276:immunology; D006801:Humans; D007515:Islets of Langerhans / Q000276:immunology*; D007564:Japan / Q000453:epidemiology; D008297:Male; D054635:Receptor-Like Protein Tyrosine Phosphatases, Class 8 / Q000276:immunology; D016036:Seroepidemiologic Studies; D013997:Time Factors; D055815:Young Adult
chemical_list: D000906:Antibodies; D001324:Autoantigens; D054635:Receptor-Like Protein Tyrosine Phosphatases, Class 8; D005968:Glutamate Decarboxylase; C401141:glutamate decarboxylase 2