ArticleNature communications2025
Imbalance of stem-like and effector T cell states in children with early type 1 diabetes across conventional and regulatory subsets.
Article in Nature communications, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 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
2 citing papers in PubMed.
- Local and circulating cytotoxic CD4medRxiv : the preprint server for health sciences · 2026Article
- Immune signaling as a determinant of cellular identity and tissue function.Frontiers in immunology · 2026Review
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Authors and funding
8 authors.
Funding
Abstract
Type 1 diabetes (T1D) is an autoimmune disease caused by the loss of self-tolerance toward insulin-producing pancreatic β-cells. Its etiology remains incompletely understood but involves dysregulated T cell responses. Here, we perform single-cell transcriptomic analysis of peripheral blood T cells from children newly diagnosed with T1D, the same children after one year, and healthy donors. We observe that children with diabetes show diminished effector and cytotoxic programs and enhanced stemness-associated gene signature across diverse T cell subsets, especially at diagnosis. In parallel, we detect signs of impaired regulatory capacity in regulatory T cells and regulatory TR3-56 cells. These findings are supported by flow cytometry analysis of the same cohort and reanalysis of publicly available datasets. Overall, our results suggest that T1D is associated with impaired T cell effector differentiation and regulatory T cell dysfunction, both of which may contribute to immune imbalance and loss of self-tolerance.
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