ArticleMetabolism open2020
Investigating the potential impact of post translational modification of auto-antigens by tissue transglutaminase on humoral islet autoimmunity in type 1 diabetes.
Article in Metabolism open, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
6 citing papers in PubMed, 6 citations in OpenAlex.
- Beyond Sequence: Posttranslational Remodeling of Antigens in Autoimmunity.Immunological reviews · 2026Review
- The role of oxidative post-translational modifications in type 1 diabetes pathogenesis.Frontiers in immunology · 2025Review
- Review
- Posttranslational modifications in diabetes: Mechanisms and functions.Reviews in endocrine & metabolic disorders · 2022Review
- Current status of PTMs structural databases: applications, limitations and prospects.Amino acids · 2022Review
- Biomarkers of autoimmunity and beta cell metabolism in type 1 diabetes.Frontiers in immunology · 2022Review
Corrections and comments
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Authors and funding
2 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundPost-translational modification (PTM) of antigens plays a role in the pathogenesis of many autoimmune disorders. In coeliac disease (CD), tissue transglutaminase (tTG) deamidates gliadin peptides to activate the immune response against the gut endomysium. CD is six times more prevalent in type 1 diabetes (T1D) patients than in the general population. HYPOTHESIS: tTG also modifies auto-antigens implicated in the pathogenesis of T1D, leading to an autoimmune response to pancreatic β-cells.
methodstTG PTM was investigated in the following auto-antigens, which had been previously shown to have high importance in the development of T1D: glutamic acid decarboxylase isoform 65 (GAD65), full length islet antigen (IA-2), intracellular portion of IA-2 (IA-2ic), and both isoforms of zinc transporter 8 (ZnT8W and ZnT8R), on antibody binding. Radiolabelled antigen was incubated with tTG for 20 h at 37 °C in 100 mM Denver buffer, 3.33 nM CaCl
resultsResults varied between serum samples. Generally, tTG treatment of ZnT8W, ZnT8R and IA-2ic showed no significant change in antigen: autoantibody binding, while increases in binding were observed with tTG-treated GAD65 and full length IA-2.
conclusionIn the case of GAD65, full length IA-2, the strength of antibody: antigen binding increased after incubation with tTG. However, the exact tTG-modification events that occurred requires further elucidation.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.