ReviewCurrent diabetes reports2015
Targeting memory T cells in type 1 diabetes.
Review in Current diabetes reports, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
25 citing papers in PubMed, 40 citations in OpenAlex.
- Modulation of Autoimmune T-Cell Memory by Stem Cell Educator Therapy: Phase 1/2 Clinical Trial.EBioMedicine · 2015Trial
- Increased expression of OX40 on peripheral CD4Acta diabetologica · 2026Article
- ST8Sia6 overexpression protects pancreatic β cells from spontaneous autoimmune diabetes in nonobese diabetic mice.The Journal of clinical investigation · 2025Article
- Single-cell multiomic analysis unveils the immune landscape dynamics of graves' ophthalmopathy.Communications biology · 2025Article
- From Edmonton to Lantidra and beyond: immunoengineering islet transplantation to cure type 1 diabetes.Frontiers in transplantation · 2025Review
- Research Advances in Fusion Protein-Based Drugs for Diabetes Treatment.Diabetes, metabolic syndrome and obesity : targets and therapy · 2024Review
- Shifts in isoform usage underlie transcriptional differences in regulatory T cells in type 1 diabetes.Communications biology · 2023Article
- Comprehensive analysis of endoplasmic reticulum stress-related mechanisms in type 2 diabetes mellitus.World journal of diabetes · 2023Article
- Pathophysiology of Type 1 Diabetes and Gut Microbiota Role.International journal of molecular sciences · 2022Review
- The frequency of CD4+ and CD8+ circulating T stem cell memory in type 1 diabetes.Immunity, inflammation and disease · 2022Article
- Autoreactive CD8 T cells in NOD mice exhibit phenotypic heterogeneity but restricted TCR gene usage.Life science alliance · 2022Article
- Article
- Chemokines in Type 1 Diabetes Mellitus.Frontiers in immunology · 2021Article
- Immune Modulation of Platelet-Derived Mitochondria on Memory CD4International journal of molecular sciences · 2020Article
- Article
- Targeting Type 1 Diabetes: Selective Approaches for New Therapies.Biochemistry · 2019Review
- Soluble CD137 Ameliorates Acute Type 1 Diabetes by Inducing T Cell Anergy.Frontiers in immunology · 2019Article
- Inhibition of C-X-C motif chemokine 10 reduces graft loss mediated by memory CD8Experimental and therapeutic medicine · 2018Article
- Harnessing the properties of dendritic cells in the pursuit of immunological tolerance.Biomedical journal · 2017Review
- Update on Dendritic Cell-Induced Immunological and Clinical Tolerance.Frontiers in immunology · 2017Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 2 institutions in 1 country.
Funding
Abstract
Type 1 diabetes (T1D) is a chronic autoimmune disease that leads to progressive destruction of pancreatic beta cells. Compared to healthy controls, a characteristic feature of patients with T1D is the presence of self-reactive T cells with a memory phenotype. These autoreactive memory T cells in both the CD4(+) and CD8(+) compartments are likely to be long-lived, strongly responsive to antigenic stimulation with less dependence on costimulation for activation and clonal expansion, and comparatively resistant to suppression by regulatory T cells (Tregs) or downregulation by immune-modulating agents. Persistence of autoreactive memory T cells likely contributes to the difficulty in preventing disease progression in new-onset T1D and maintaining allogeneic islet transplants by regular immunosuppressive regimens. The majority of immune interventions that have demonstrated some success in preserving beta cell function in the new-onset period have been shown to deplete or modulate memory T cells. Based on these and other considerations, preservation of residual beta cells early after diagnosis or restoration of beta cell mass by use of stem cell or transplantation technology will require a successful strategy to control the autoreactive memory T cell compartment, which could include depletion, inhibition of homeostatic cytokines, induction of hyporesponsiveness, or a combination of these approaches.
Indexed as
Identifiers
What OpenQuestion holds
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.