Evidence map›Paper›PMID 41197380›Full record

ArticleEBioMedicine2025

Blimp-1 benefits gut-homing regulatory T cells by maintaining migration/suppressive function in autoimmune diabetes-prone mice.

Yi-Wen Tsai, Yu-Wen Liu, Chao-Yuan Hsu, Shin-Huei Fu, Ming-Wei Chien, Jia-Ling Dong, Chi-Chin Sun, Chien-Tzung Chen, Huey-Kang Sytwu

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Article in EBioMedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

The trial behind it

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Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

9 authors.

Yi-Wen TsaiGraduate Institute of Medical Sciences, National Defense Medical University, No. 161, Section 6, Min Chuan East Road, Neihu, Taipei, 114, Taiwan; Department of Family Medicine, Chang Gung Memorial Hospital, Linkou, No. 5, Fuxing St., Guishan Dist., Taoyuan City, 333, Taiwan; Department of Family Medicine, New Taipei Municipal Tucheng Hospital (Bulit and Operated by Chang Gung Medical Foundation), No. 6, Section 2, Jincheng Road, Tucheng District, New Taipei City, 236, Taiwan; School of Medicine, College of Medicine, Chang-Gung University, No. 259, Wenhua 1st Road, Guishan District, Taoyuan City, 333, Taiwan.
Yu-Wen LiuGraduate Institute of Microbiology and Immunology, National Defense Medical University, No. 161, Section 6, Min Chuan East Road, Neihu, Taipei, 114, Taiwan; National Institute of Infectious Diseases and Vaccinology, National Health Research Institutes, No. 35, Keyan Road, Zhunan, Miaoli, 350, Taiwan.
Chao-Yuan HsuGraduate Institute of Microbiology and Immunology, National Defense Medical University, No. 161, Section 6, Min Chuan East Road, Neihu, Taipei, 114, Taiwan.
Shin-Huei FuGraduate Institute of Microbiology and Immunology, National Defense Medical University, No. 161, Section 6, Min Chuan East Road, Neihu, Taipei, 114, Taiwan; National Institute of Infectious Diseases and Vaccinology, National Health Research Institutes, No. 35, Keyan Road, Zhunan, Miaoli, 350, Taiwan.
Ming-Wei ChienGraduate Institute of Microbiology and Immunology, National Defense Medical University, No. 161, Section 6, Min Chuan East Road, Neihu, Taipei, 114, Taiwan; National Institute of Infectious Diseases and Vaccinology, National Health Research Institutes, No. 35, Keyan Road, Zhunan, Miaoli, 350, Taiwan.
Jia-Ling DongGraduate Institute of Life Sciences, National Defense Medical University, No. 161, Section 6, Min Chuan East Road, Neihu, Taipei, 114, Taiwan.
Chi-Chin SunSchool of Medicine, College of Medicine, Chang-Gung University, No. 259, Wenhua 1st Road, Guishan District, Taoyuan City, 333, Taiwan; Department of Ophthalmology, Chang Gung Memorial Hospital, Keelung, No. 222, Maijin Road, Keelung, 204, Taiwan.
Chien-Tzung ChenSchool of Medicine, College of Medicine, Chang-Gung University, No. 259, Wenhua 1st Road, Guishan District, Taoyuan City, 333, Taiwan; Department of Plastic and Reconstruction Surgery, Chang Gung Memorial Hospital, Linkou, No. 5, Fuxing St., Guishan Dist., Taoyuan City, 333, Taiwan.
Huey-Kang SytwuGraduate Institute of Medical Sciences, National Defense Medical University, No. 161, Section 6, Min Chuan East Road, Neihu, Taipei, 114, Taiwan; Graduate Institute of Microbiology and Immunology, National Defense Medical University, No. 161, Section 6, Min Chuan East Road, Neihu, Taipei, 114, Taiwan; National Institute of Infectious Diseases and Vaccinology, National Health Research Institutes, No. 35, Keyan Road, Zhunan, Miaoli, 350, Taiwan; Graduate Institute of Life Sciences, National Defense Medical University, No. 161, Section 6, Min Chuan East Road, Neihu, Taipei, 114, Taiwan. Electronic address: sytwu@nhri.org.tw.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

backgroundGenome-wide association studies (GWAS) have shown that Crohn's disease (CD) and type 1 diabetes (T1D) are the top 2 diseases with the highest genetic risk variants and share several susceptible loci. Since both CD and T1D are T cell-mediated diseases, we hypothesise a mechanistic linkage between T-cell homeostasis and a gut-pancreas axis that differentially regulates the immunopathogenesis and development between CD and T1D.

methodsUsing data for 1 million people from a 16-year nationwide population-based databank in Taiwan, we unraveled a higher risk of prevalent inflammatory bowel disease in T1D patients. This observation is supported by our model of T-cell-specific B-lymphocyte-induced maturation protein 1 (Blimp-1) deficiency-induced colitis, in which more severe colitogenesis was observed in diabetes-prone non-obese diabetic (NOD) mice than in non-diabetes-prone C57BL/6 mice.

findingsMechanistic investigations revealed that, compared with Tregs in C57BL/6 background, those in Blimp-1-deficient NOD mice exhibited decreased suppressive function, increased TCR signaling strength and impaired intestinal migration, particularly for gut-homing Th17-like Tregs. Strikingly, transgenic augmentation of PEST domain-enriched tyrosine phosphatase (Pep) to downregulate TCR signaling strength reversed exacerbated colitis and increased disease-free percentage of Blimp-1-deficient NOD mice. Adoptive transfer experiments further supported that Pep overexpression restored suppressive function of fragilized Tregs in Blimp-1-deficient NOD mice.

interpretationOur results demonstrate that Blimp-1 sustains the suppressive function of gut-homing Tregs and that Pep-based TCR signaling manipulation may serve as a therapeutic target in autoimmune diseases.

fundingThis study was funded by the Ministry of Science and Technology, Taiwan (MOST109-2320-B-400-018-MY3, MOST110-2320-B-400-011-MY3, MOST109-2314-B-182A-149); the National Science and Technology Council, Taiwan (NSTC112-2320-B-400-026-MY3, NSTC113-2320-B-400-019-MY3); the Tri-Service General Hospital (TSGH-C02-112029, TSGH-C03-113037, TSGH-C01-114028, VTA112-T-1-1, VTA113-T-1-1); and the Chang Gung Memorial Hospital Research Projects (NMRPG2K0021, CMRPG2M0041, CMRPVVM0182, CORPVVN0131, CMRPG2I0071, CMRPG2I0072, CMRPG2I0073, CORPG3P0622).

Indexed as

Cell MovementDiabetes Mellitus, Type 1Positive Regulatory Domain I-Binding Factor 1T-Lymphocytes, RegulatoryAnimalsDisease Models, AnimalFemaleHumansMiceMice, Inbred NODPositive Regulatory Domain I-Binding Factor 1Prdm1 protein, mouseBlimp-1CCR6(+)RORγt(+) Th17-like Treg cellsCrohn's diseaseGut-homing regulatory T cellsT-cell receptor signaling strengthType 1 diabetes

Identifiers

PMID41197380
PMCPMC12636379

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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.