---
title: "Treg and Teff Transcriptional Shifts in Type 1 Diabetes Mellitus"
id: "pubmed-42920033"
canonical_url: "https://medichelpline.com/clinical-feed/pubmed-42920033"
content_type: "clinical_feed_article"
specialty: "Pharmacology"
source_name: "PubMed / NCBI"
source_url: "https://pubmed.ncbi.nlm.nih.gov/42920033/"
doi: "10.1186/s43556-026-00636-9"
published_at: "2026-10-24T00:00:00.000Z"
evidence_level: "Journal Article"
license: "CC-BY-NC-4.0 / Informational Use"
---
# Treg and Teff Transcriptional Shifts in Type 1 Diabetes Mellitus
## Provenance & Clinical Metadata
- **Canonical URL:** https://medichelpline.com/clinical-feed/pubmed-42920033
- **Specialty:** [Pharmacology](https://medichelpline.com/clinical-feed/pharmacology.md)
- **Primary Source:** PubMed / NCBI
- **Source URL:** [Original Journal Publication](https://pubmed.ncbi.nlm.nih.gov/42920033/)
- **DOI:** [10.1186/s43556-026-00636-9](https://doi.org/10.1186%2Fs43556-026-00636-9)
- **Published At:** 2026-10-24T00:00:00.000Z
- **Evidence Rating:** Journal Article
## Executive GIST (TL;DR)
- The authors investigated T-cell dysregulation in a streptozotocin (STZ)-induced **Type 1 diabetes mellitus** mouse model using integrated transcriptomics, flow cytometry, glycemic correlation, and cross-model validation. - Regulatory T cells (**Tregs**) in T1DM showed proliferative and effector-like transcriptional signatures, with increased Melk, Prf1, Gzma and Hk2 expression and decreased Tnfsf15, Irak3 and Zeb2. - Transcription-factor networks involving Nfatc2, Elk1 and Ahr were altered in the Treg compartment, indicating lineage instability and metabolic reprogramming. - Flow cytometry found a higher frequency of splenic **Tregs**, broad upregulation of checkpoint receptors PD-1, TIGIT, LAG3 and TIM3, reduced GARP and LAP, and increased IL-17 and IFN-γ production. - Effector T cells (Teffs) exhibited hyperactivation accompanied by transcriptional imbalance; the study team described these changes but did not report additional mechanistic or dosing details. - Cross-model analyses across C57BL/6, NOD, and human datasets revealed concordant IL-15, IL-36A, E2F and metabolic programs and shared genes Smad3, Mki67 and Cxcr4. - The cohort-level data suggest Treg phenotypes combining high checkpoint expression and inflammatory features that could affect immune tolerance in T1DM. - All experiments used mice; the authors confirmed institutional ethics approval and stated no human subjects were involved. The paper did not report clinical dosing, patient demographics, or therapeutic interventions.
## Clinical Analysis & Structured Key Points
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Affiliations Expand ### Affiliations * 1 Centre of Excellence for Oncology and Immunology, Academy of Life and Natural Sciences, Xi'an Jiaotong-Liverpool University, No. 111 Ren'ai Road, Suzhou, 215123, China. * 2 Centre of Excellence for Oncology and Immunology, Academy of Life and Natural Sciences, Xi'an Jiaotong-Liverpool University, No. 111 Ren'ai Road, Suzhou, 215123, China. eyad.elkord@xjtlu.edu.cn. * 3 Biomedical Research Center, School of Science, Engineering and Environment, University of Salford, Manchester, M5 4WT, UK. eyad.elkord@xjtlu.edu.cn. * PMID: **42920033** * DOI: [ 10.1186/s43556-026-00636-9 ](https://doi.org/10.1186/s43556-026-00636-9) Item in Clipboard # Transcriptional and phenotypic alterations of regulatory and effector T cells in type 1 diabetes mellitus Yutong Li et al. Mol Biomed. 2026. Show details Display options Display options Format Abstract PubMed PMID Mol Biomed Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Mol+Biomed%22%5Bjour%5D&sort=date&sort_order=desc) * [ Search in NLM Catalog ](https://www.ncbi.nlm.nih.gov/nlmcatalog?term=%22Mol+Biomed%22%5BTitle+Abbreviation%5D) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42920033/) . 2026 Oct 24;7(1):227. doi: 10.1186/s43556-026-00636-9. ### Authors [Yutong Li](https://pubmed.ncbi.nlm.nih.gov/?term=Li+Y&cauthor_id=42920033)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42920033/#short-view-affiliation-1 "Centre of Excellence for Oncology and Immunology, Academy of Life and Natural Sciences, Xi'an Jiaotong-Liverpool University, No. 111 Ren'ai Road, Suzhou, 215123, China."), [Xinhui Zhao](https://pubmed.ncbi.nlm.nih.gov/?term=Zhao+X&cauthor_id=42920033)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42920033/#short-view-affiliation-1 "Centre of Excellence for Oncology and Immunology, Academy of Life and Natural Sciences, Xi'an Jiaotong-Liverpool University, No. 111 Ren'ai Road, Suzhou, 215123, China."), [Mingxin Xie](https://pubmed.ncbi.nlm.nih.gov/?term=Xie+M&cauthor_id=42920033)[ 1 ](https://pubmed.ncbi.nlm.nih.gov/42920033/#short-view-affiliation-1 "Centre of Excellence for Oncology and Immunology, Academy of Life and Natural Sciences, Xi'an Jiaotong-Liverpool University, No. 111 Ren'ai Road, Suzhou, 215123, China."), [Eyad Elkord](https://pubmed.ncbi.nlm.nih.gov/?term=Elkord+E&cauthor_id=42920033)[ 2 ](https://pubmed.ncbi.nlm.nih.gov/42920033/#short-view-affiliation-2 "Centre of Excellence for Oncology and Immunology, Academy of Life and Natural Sciences, Xi'an Jiaotong-Liverpool University, No. 111 Ren'ai Road, Suzhou, 215123, China. eyad.elkord@xjtlu.edu.cn.")[ 3 ](https://pubmed.ncbi.nlm.nih.gov/42920033/#short-view-affiliation-3 "Biomedical Research Center, School of Science, Engineering and Environment, University of Salford, Manchester, M5 4WT, UK. eyad.elkord@xjtlu.edu.cn.") ### Affiliations * 1 Centre of Excellence for Oncology and Immunology, Academy of Life and Natural Sciences, Xi'an Jiaotong-Liverpool University, No. 111 Ren'ai Road, Suzhou, 215123, China. * 2 Centre of Excellence for Oncology and Immunology, Academy of Life and Natural Sciences, Xi'an Jiaotong-Liverpool University, No. 111 Ren'ai Road, Suzhou, 215123, China. eyad.elkord@xjtlu.edu.cn. * 3 Biomedical Research Center, School of Science, Engineering and Environment, University of Salford, Manchester, M5 4WT, UK. eyad.elkord@xjtlu.edu.cn. * PMID: **42920033** * DOI: [ 10.1186/s43556-026-00636-9 ](https://doi.org/10.1186/s43556-026-00636-9) Item in Clipboard Cite Display options Display options Format Abstract PubMed PMID Linked Discoveries ## Abstract Type 1 diabetes mellitus (T1DM) is characterized by the destruction of pancreatic β-cells, in which the dysfunction of regulatory T cells (Tregs) contributes to impaired immune tolerance. However, Treg heterogeneity remains incompletely understood, which limits the effectiveness of current therapies. Here, we have integrated transcriptome, flow cytometry, glycemic correlation, and cross-model validation to characterize the dysregulation of Tregs and effector T cells (Teffs) in a streptozotocin (STZ)-induced T1DM mouse model. Tregs exhibited a proliferative, effector-like, unstable lineage, and metabolic reprogramming features, marked by increased Melk, Prf1, Gzma and Hk2, and decreased expression of Tnfsf15, Irak3 and Zeb2 in T1DM, and alterations in the transcription-factor networks involving Nfatc2, Elk1, and Ahr. Flow cytometry further revealed that the frequency of splenic Tregs was significantly increased, accompanied by broad upregulation of programmed cell death protein 1 (PD-1), T cell immunoreceptor with Ig and ITIM domains (TIGIT), lymphocyte-activation gene 3 (LAG3), and T-cell immunoglobulin and mucin domain-containing protein 3 (TIM3). Meanwhile, expression of glycoprotein A repetitions predominant (GARP) and latency-associated peptide (LAP) was decreased, whereas interleukin (IL)- 17 and interferon-γ (IFN-γ) secretion were increased, suggesting a Treg phenotype with high checkpoint expression and inflammatory features. Cross-model analyses identified concordant IL-15-, IL-36 A-, E2F-, and metabolic programs across the C57BL/6, non-obese diabetic (NOD), and human datasets, including shared genes Smad3, Mki67, and Cxcr4. Teffs also displayed a hyperactivated but transcriptionally imbalanced phenotype in T1DM. Collectively, our findings reveal transcriptional and phenotypic alterations in Tregs and Teffs, providing new insights into T-cell dysregulation and potentially informing the development of Treg-based immunotherapies in T1DM. **Keywords:** Immune checkpoints; Inflammation; Transcriptional profiling; Tregs; Type 1 diabetes mellitus. © 2026. The Author(s). [PubMed Disclaimer](https://pubmed.ncbi.nlm.nih.gov/disclaimer/) ## Conflict of interest statement Declarations. Ethics approval and consent to participate: All animal experiments were performed in accordance with the guidelines of National General Requirements for Animal Experiment (GB/T 35823–2018) and the protocol approved by the University Research Ethics Review Panel of Xi’an Jiaotong-Liverpool University (Approval No.: ER-SRR-11000161020241017103725; date: 22 October 2024). No human subjects were involved in this study; therefore, informed consent from patients was not required. Consent for publication: Not applicable. Competing interests: The authors have no relevant financial or non-financial interests to disclose. ## References 1. 1. Norris JM, Johnson RK, Stene LC. Type 1 diabetes—early life origins and changing epidemiology. Lancet Diabetes Endocrinol. 2020;8(3):226–38. . - [DOI](https://doi.org/10.1016/s2213-8587\(19\)30412-7) - [PubMed](https://pubmed.ncbi.nlm.nih.gov/31999944/) - [PMC](https://pmc.ncbi.nlm.nih.gov/articles/7332108/) 2. 1. Gregory GA, Robinson TIG, Linklater SE, Wang F, Colagiuri S, de Beaufort C, et al. Global incidence, prevalence, and mortality of type 1 diabetes in 2021 with projection to 2040: a modelling study. Lancet Diabetes Endocrinol. 2021;10(10):741–60. . - [DOI](https://doi.org/10.1016/s2213-8587\(22\)00218-2) 3. 1. Ogle GD, Wang F, Haynes A, Gregory GA, King TW, Deng K, et al. Global type 1 diabetes prevalence, incidence, and mortality estimates 2025: results from the International Diabetes Federation Atlas, 11th Edition, and the T1D Index Version 3.0. Diabetes Res Clin Pract. 2025;225:112277. . - [DOI](https://doi.org/10.1016/j.diabres.2025.112277) - [PubMed](https://pubmed.ncbi.nlm.nih.gov/40412624/) 4. 1. ElSayed NA, McCoy RG, Aleppo G, Bajaj M, Balapattabi K, Beverly EA, et al. Pharmacologic approaches to glycemic treatment: standards of care in diabetes—2025. Diabetes Care. 2025;48(Suppl 1):S181–206. . - [DOI](https://doi.org/10.2337/dc25-s009) 5. 1. Larsen R, Taylor F, Dempsey PC, McNarry M, Rickards K, Sethi P, et al. Effect of interrupting prolonged sitting with frequent activity breaks on postprandial glycemia and insulin sensitivity in adults with type 1 diabetes on continuous subcutaneous insulin infusion therapy: a randomized crossover pilot trial. Diabetes Technol Ther. 2025;27(2):101–12. . - [DOI](https://doi.org/10.1089/dia.2024.0146) - [PubMed](https://pubmed.ncbi.nlm.nih.gov/39506625/) Show all 61 references ## MeSH terms * Animals Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Animals%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Animals) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42920033/) * Diabetes Mellitus, Experimental / genetics Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Diabetes+Mellitus%2C+Experimental%2Fgenetics%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Diabetes+Mellitus%2C+Experimental) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42920033/) * Diabetes Mellitus, Experimental / immunology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Diabetes+Mellitus%2C+Experimental%2Fimmunology%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Diabetes+Mellitus%2C+Experimental) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42920033/) * Diabetes Mellitus, Type 1* / genetics Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Diabetes+Mellitus%2C+Type+1%2Fgenetics%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Diabetes+Mellitus%2C+Type+1) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42920033/) * Diabetes Mellitus, Type 1* / immunology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Diabetes+Mellitus%2C+Type+1%2Fimmunology%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Diabetes+Mellitus%2C+Type+1) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42920033/) * Diabetes Mellitus, Type 1* / pathology Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Diabetes+Mellitus%2C+Type+1%2Fpathology%22%5BMAJR%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Diabetes+Mellitus%2C+Type+1) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42920033/) * Gene Expression Profiling Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Gene+Expression+Profiling%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Gene+Expression+Profiling) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42920033/) * Male Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Male%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Male) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42920033/) * Mice Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Mice%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Mice) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42920033/) * Mice, Inbred C57BL Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Mice%2C+Inbred+C57BL%22%5BMeSH%5D&sort=date&sort_order=desc) * [ Search in MeSH ](https://www.ncbi.nlm.nih.gov/mesh?term=Mice%2C+Inbred+C57BL) * [ Add to Search ](https://pubmed.ncbi.nlm.nih.gov/42920033/) * Phenotype Actions * [ Search in PubMed ](https://pubmed.ncbi.nlm.nih.gov/?term=%22Phenotype%22%5BMeSH%5D&sort=date&sort_order=des
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