ArticleBMC immunology2011
Detection of autoantibodies against reactive oxygen species modified glutamic acid decarboxylase-65 in type 1 diabetes associated complications.
Article in BMC immunology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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13 citing papers in PubMed, 27 citations in OpenAlex.
- Glycation and Oxidative Stress Increase Autoantibodies in the Elderly.Molecules (Basel, Switzerland) · 2020Trial
- Molecular and Inflammatory Etiologies of β-Cell Dysfunction in Type 1 Diabetes.Physiology (Bethesda, Md.) · 2025Review
- Assessment for Diabetic Neuropathy: Treatment and Neurobiological Perspective.Current diabetes reviews · 2025Review
- Adverse effect propensity: A new feature of Gulf War illness predicted by environmental exposures.iScience · 2023Article
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- Increased inflammatory cytokines and oxidative stress enhanced antibody production in breast and prostate cancer patients with COVID-19 related depression.Frontiers in chemistry · 2023Article
- Biophysical, Biochemical, and Molecular Docking Investigations of Anti-Glycating, Antioxidant, and Protein Structural Stability Potential of Garlic.Molecules (Basel, Switzerland) · 2022Article
- New Advances on Pathophysiology of Diabetes Neuropathy and Pain Management: Potential Role of Melatonin and DPP-4 Inhibitors.Frontiers in pharmacology · 2022Review
- Seroprevalence of Anti-S1-RBD Antibodies in Pre-pandemic and Pandemic Subjects From Hail Region, KSA.Frontiers in public health · 2022Article
- Article
- Antihyperglycemic Potential of Grewia asiatica Fruit Extract against Streptozotocin-Induced Hyperglycemia in Rats: Anti-Inflammatory and Antioxidant Mechanisms.Oxidative medicine and cellular longevity · 2015Article
- The role of reactive oxygen species and proinflammatory cytokines in type 1 diabetes pathogenesis.Annals of the New York Academy of Sciences · 2013Review
- HLA-dependent autoantibodies against post-translationally modified collagen type II in type 1 diabetes mellitus.Diabetologia · 2013Article
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Authors and funding
4 authors at 2 institutions in 3 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundAutoantibodies against glutamate decarboxylase-65 (GAD₆₅Abs) are thought to be a major immunological tool involved in pathogenic autoimmunity development in various diseases. GAD₆₅Abs are a sensitive and specific marker for type 1 diabetes (T1D). These autoantibodies can also be found in 6-10% of patients classified with type 2 diabetes (T2D), as well as in 1-2% of the healthy population. The latter individuals are at low risk of developing T1D because the prevalence rate of GAD₆₅Abs is only about 0.3%. It has, therefore, been suggested that the antibody binding to GAD₆₅ in these three different GAD₆₅Ab-positive phenotypes differ with respect to epitope specificity. The specificity of reactive oxygen species modified GAD₆₅ (ROS-GAD₆₅) is already well established in the T1D. However, its association in secondary complications of T1D has not yet been ascertained. Hence this study focuses on identification of autoantibodies against ROS-GAD₆₅ (ROS-GAD₆₅Abs) and quantitative assays in T1D associated complications.
resultsFrom the cohort of samples, serum autoantibodies from T1D retinopathic and nephropathic patients showed high recognition of ROS-GAD₆₅ as compared to native GAD₆₅ (N-GAD₆₅). Uncomplicated T1D subjects also exhibited reactivity towards ROS-GAD65. However, this was found to be less as compared to the binding recorded from complicated subjects. These results were further proven by competitive ELISA estimations. The apparent association constants (AAC) indicate greater affinity of IgG from retinopathic T1D patients (1.90 x 10⁻⁶ M) followed by nephropathic (1.81 x 10⁻⁶ M) and uncomplicated (3.11 x 10⁻⁷ M) T1D patients for ROS-GAD₆₅ compared to N-GAD₆₅.
conclusionIncreased oxidative stress and blood glucose levels with extended duration of disease in complicated T1D could be responsible for the gradual formation and/or exposing cryptic epitopes on GAD₆₅ that induce increased production of ROS-GAD₆₅Abs. Hence regulation of ROS-GAD₆₅Abs could offer novel tools for analysing and possibly treating T1D complications.
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