WHAT IS A CELL
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Autoimmunity to the islets may lead to β-cell dysfunction in type 2 diabetes (T2D). However, its frequency and clinical relevance have yet to be identified. For a study, researchers assessed the incidence of cellular and humoral islet autoimmunity in individuals with T2D for 4.0±3.0 years (HbA1c 7.5± 0.5% on metformin alone) in auxiliary research to the Glycemia Reduction Approaches in Diabetes: A Comparative Effectiveness Study (GRADE).
T-cell autoreactivity against islet proteins, islet autoantibodies against the 65-kDa GAD antigen, IA-2, and zinc transporter-8, and β-cell function were all assessed. 41.3% had cellular islet autoimmune, 13.5% had humoral islet autoimmunity, and 5.3% had both. β-Cell function (iAUC-CG) and C-peptide(0–30)/glucose(0–30) from an oral glucose tolerance test were lower in T-cell–positive (T+) than T-cell–negative (T) individuals using two different adjustments for insulin sensitivity (iAUC-CG: 13.2% [95% CI 0.3, 24.4] or 11.4% [95% CI 0.4, 21.2] lower; C-peptide[0– T+ patients had a 17% higher HbA1c (95% CI 0.07, 0.28) and 7.7 mg/dL higher fasting plasma glucose levels (95% CI 0.2, 15.3) than T patients.
They concluded that islet autoimmunity was far more common in T2D patients than previously thought. Furthermore, autoimmunity mediated by T cells was linked to decreased β-cell function and poor glycemic management.