ArticleBMJ open diabetes research & care2020
Proinsulin-specific T regulatory cells may control immune responses in type 1 diabetes: implications for adoptive therapy.
Article in BMJ open diabetes research & care, 2020. 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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Who cites it
13 citing papers in PubMed, 16 citations in OpenAlex.
- Reduced TIGIT Expression on T Cells Links Hyperglycemia to Immune Dysregulation in Type 1 Diabetes.Cells · 2026Article
- Regulatory T cell therapies: biological foundations, engineering strategies, and clinical translation.Frontiers in immunology · 2026Review
- Analysis of frequency changes in CD8Diabetology & metabolic syndrome · 2024Article
- Autoimmunity and Carcinogenesis: Their Relationship under the Umbrella of Autophagy.Biomedicines · 2023Review
- Leukocytic dysregulation in children with type 1 diabetes: relation to diabetic vascular complications.Diabetology international · 2022Article
- Autoimmunity and Cancer-Two Sides of the Same Coin.Frontiers in immunology · 2022Review
- Mechanisms and therapeutic strategies of immune checkpoint molecules and regulators in type 1 diabetes.Frontiers in endocrinology · 2022Review
- Potential Therapeutic Application of Regulatory T Cells in Diabetes Mellitus Type 1.International journal of molecular sciences · 2021Review
- Successful Treatment of Persistent SARS-CoV-2 Infection in a B-Cell Depleted Patient with Activated Cytotoxic T and NK Cells: A Case Report.International journal of molecular sciences · 2021Article
- Paving the way towards an effective treatment for multiple sclerosis: advances in cell therapy.Cellular & molecular immunology · 2021Review
- Exploiting Single-Cell Tools in Gene and Cell Therapy.Frontiers in immunology · 2021Review
- Intestinal Microbiota in Common Chronic Inflammatory Disorders Affecting Children.Frontiers in immunology · 2021Review
- Antigenic Challenge Influences Epigenetic Changes in Antigen-Specific T Regulatory Cells.Frontiers in immunology · 2021Article
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Authors and funding
21 authors at 5 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
objectiveHere we looked for possible mechanisms regulating the progression of type 1 diabetes mellitus (T1DM). In this disease, autoaggressive T cells (T conventional cells, Tconvs) not properly controlled by T regulatory cells (Tregs) destroy pancreatic islets. RESEARCH DESIGN AND
methodsWe compared the T-cell compartment of patients with newly diagnosed T1DM (NDT1DM) with long-duration T1DM (LDT1DM) ones. The third group consisted of patients with LDT1DM treated previously with polyclonal Tregs (LDT1DM with Tregs). We have also looked if the differences might be dependent on the antigen specificity of Tregs expanded for clinical use and autologous sentinel Tconvs.
resultsPatients with LDT1DM were characterized by T-cell immunosenescence-like changes and expansion of similar vβ/T-cell receptor (TCR) clones in Tconvs and Tregs. The treatment with Tregs was associated with some inhibition of these effects. Patients with LDT1DM possessed an increased percentage of various proinsulin-specific T cells but not GAD65-specific ones. The percentages of all antigen-specific subsets were higher in the expansion cultures than in the peripheral blood. The proliferation was more intense in proinsulin-specific Tconvs than in specific Tregs but the levels of some proinsulin-specific Tregs were exceptionally high at baseline and remained higher in the expanded clinical product than the levels of respective Tconvs in sentinel cultures.
conclusionsT1DM is associated with immunosenescence-like changes and reduced diversity of T-cell clones. Preferential expansion of the same TCR families in both Tconvs and Tregs suggests a common trigger/autoantigen responsible. Interestingly, the therapy with polyclonal Tregs was associated with some inhibition of these effects. Proinsulin-specific Tregs appeared to be dominant in the immune responses in patients with T1DM and probably associated with better control over respective autoimmune Tconvs. TRIAL REGISTRATION NUMBER: EudraCT 2014-004319-35.
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