Pöllänen PM, Härkönen T, Ilonen J, et al. - In this cross-sectional study, the role of autoantibodies to N-terminally truncated glutamic acid decarboxylase GAD65(96–585) (t-GADA) as a marker for type 1 diabetes (T1D) was examined. In addition, the potential HLA-associations with such autoantibodies were determined.

• Data from the Finnish Pediatric Diabetes Register, the Type 1 Diabetes Prediction and Prevention (DIPP) Study, the DIABIMMUNE Study, and the Early Dietary Intervention and Later Signs of Beta-Cell Autoimmunity (EDIA) Study were collated.

• t-GADA, autoantibodies to full-length GAD₆₅ (f-GADA), and islet cell antibodies were analyzed in venous blood samples obtained from 760 individuals (53.7% males).

• Assessment of epitope-specific GAD autoantibodies was done in 189 study participants.

• There appeared an improvement in the screening for T1D in correlation with using autoantibodies to N-terminally truncated GAD vs f-GADA, that may facilitate the selection of participants for clinical trials.

• A possible relevant pathomechanism in T1D is HLA class II-mediated antigen presentation of GAD (96–585)-derived or structurally similar peptides.