Protein Information

ID 2961
Name glutamic acid decarboxylase
Synonyms 65 kDa glutamic acid decarboxylase; GAD 2; GAD 65; GAD2; GAD65; Glutamate decarboxylase 2; Glutamate decarboxylase 2 (pancreas); Glutamate decarboxylase 65 kDa isoform…

Compound Information

ID 1689
Name IAA
CAS

Reference

PubMed Abstract RScore(About this table)
11353881 Monge L, Pinach S, Caramellino L, Bertero MT, Dall'omo A, Carta Q: The possible role of autoimmunity in the pathogenesis of diabetes in B-thalassemia major. Diabetes Metab. 2001 Apr;27(2 Pt 1):149-54.
OBJECTIVE: To evaluate the possible role of autoimmunity in the pathogenesis of diabetes associated with B-thalassemia, we studied a cohort of 53 B-thalassemic individuals, under long term blood transfusion, that included twelve patients with diabetes (22.6%). MATERIAL AND METHODS: To evaluate the activation of an autoimmune response, individuals were tested for islet cell antibodies (ICA), glutamic acid decarboxylase (GAD) autoantibodies, insulin autoantibodies (IAA) and serum anti-nuclear antibodies (ANA). RESULTS: Nine of the total B-thalassemic population (16.98%) were ICA-positive. The frequency of ICA-positive subjects among thalassemic individuals was higher than in the general population. Five (41.6%) of the ICA-positive individuals were diabetic. Of these, three were serum C-peptide-negative (<0.21 nmol/l). HLA class II typing of our thalassemic population did not reveal significantly different allelic frequencies with respect to the control population. CONCLUSIONS: Our study demonstrates evidence of immune system activation against pancreatic B-cells in B-thalassemia and we propose that iron deposition may, through oxidative damage, act as an environmental factor that triggers the autoimmune response. Therefore, we speculate that pancreatic autoimmunity may contribute to selective B-cells damage in the pathogenesis of diabetes associated with B-thalassemia.
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