ReviewFrontiers in endocrinology2025
Regulatory T cell dysfunction and immunotherapeutic breakthroughs in type 1 diabetes.
Review in Frontiers in endocrinology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 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
5 citing papers in PubMed.
- Review
- Artificial intelligence-driven therapeutics for disease modification in type 1 diabetes: a digital public health and clinical translation framework.Frontiers in public health · 2026Review
- Combination of proton-pump inhibitor and anti-CD3 F(ab')Immunotherapy advances · 2026Article
- Nardilysin: classical functions and new horizons in autoimmunity.Frontiers in immunology · 2026Review
- Regulatory T Cells in Diabetic Wound Healing: A Comprehensive Review.Journal of inflammation research · 2026Review
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Type 1 diabetes (T1D) is characterized by the autoimmune destruction of insulin-producing β-cells in the pancreas. Regulatory T cells (Tregs) are essential for maintaining immune tolerance, but they manifest impaired functionality, particularly within the pancreatic microenvironment, during T1D development. This review aimed to discuss Treg biology including the developmental trajectory, phenotypic heterogeneity, and suppressive function, by which we sought to emphasize their compromised role in T1D pathogenesis associated with genetic/epigenetic factors along with impaired cytokine signaling. The unique chemokine receptor expression signature, migratory capacity, and metabolic adaptation of pancreatic Tregs are highlighted, alongside insights from single-cell studies. The evolution of Treg-based immunotherapies is explored, with emphasis on genetically engineered Tregs (EngTregs), which are designed for the stable ectopic expression of FoxP3 and antigen-specific receptors, such as T cell receptors (TCR) or chimeric antigen receptors (CAR). It also highlights advancements in genome-editing and delivery technologies, along with rationally designed combination strategies incorporated into multifunctional cellular products. Despite encouraging preclinical results, significant challenges persist in clinical translation. Overall, this review synthesizes existing knowledge and outlines future directions in Treg biology and immunotherapy, underscoring the potential of next-generation Treg therapy to achieve durable immune tolerance in T1D.
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.