Evidence map›Paper›PMID 40213561›Full record

ArticleFrontiers in immunology2025

Polarization of Vδ2 T cells to a Th2-like phenotype promotes plasmablast differentiation and possesses pro-fibrotic properties in IgG4-related disease.

Jieqiong Li, Mu Wang, Jiaxin Zhou, Yunyun Fei, Mengtao Li, Yan Zhao, Xiaofeng Zeng, Linyi Peng, Wen Zhang

Abstract read
In one paragraph

Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
1 · What the graph read from it

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.

2 · The registry

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.

3 · Its place in the literature

Who cites it

2 citing papers in PubMed.

  1. Article
  2. 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.

Jieqiong LiDepartment of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases, State Key Laboratory of Complex Severe and Rare Diseases, The Ministry of Education Key Laboratory, Beijing, China.
Mu WangDepartment of Stomatology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Beijing, China.
Jiaxin ZhouDepartment of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases, State Key Laboratory of Complex Severe and Rare Diseases, The Ministry of Education Key Laboratory, Beijing, China.
Yunyun FeiDepartment of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases, State Key Laboratory of Complex Severe and Rare Diseases, The Ministry of Education Key Laboratory, Beijing, China.
Mengtao LiDepartment of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases, State Key Laboratory of Complex Severe and Rare Diseases, The Ministry of Education Key Laboratory, Beijing, China.
Yan ZhaoDepartment of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases, State Key Laboratory of Complex Severe and Rare Diseases, The Ministry of Education Key Laboratory, Beijing, China.
Xiaofeng ZengDepartment of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases, State Key Laboratory of Complex Severe and Rare Diseases, The Ministry of Education Key Laboratory, Beijing, China.
Linyi PengDepartment of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases, State Key Laboratory of Complex Severe and Rare Diseases, The Ministry of Education Key Laboratory, Beijing, China.
Wen ZhangDepartment of Rheumatology and Clinical Immunology, Peking Union Medical College Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, National Clinical Research Center for Dermatologic and Immunologic Diseases, State Key Laboratory of Complex Severe and Rare Diseases, The Ministry of Education Key Laboratory, Beijing, China.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Objectives: To explore the phenotype and role of gamma delta (γδ) T cells in the pathogenesis of IgG4-related disease (IgG4-RD). Methods: Flow cytometry and quantitative RT-PCR were employed to analyze γδ T cell subsets, chemokine receptor expression, cytokine production, pro-fibrotic gene expression, and transcription factor profiles. Immunofluorescence assessed Vδ2 T cell infiltration in affected tissues. Chemotaxis assays and co-culture experiments investigated Vδ2 T cell migration and their influence on B cell differentiation. The impact of IL-21 stimulation and JAK/STAT3 inhibitors on γδ T cell was also evaluated. Results: Patients with IgG4-RD exhibited decreased peripheral Vδ2 T cells displaying a Th2-like phenotype characterized by elevated Th2 cytokine production and activated IL-21-STAT3-Blimp-1-GATA3 pathway. Vδ2 T cells accumulated in affected tissues through CCR7 upregulation, and co-localizing with B cells. Both Vδ2 T cells and culture supernatants from IgG4-RD patients promoted B cell differentiation. IL-21 stimulation augmented pSTAT3, Blimp-1, and GATA3 expression in Vδ2 T cells, while JAK and STAT3 inhibitors attenuated these effects. IgG4-RD patients exhibited increased TGF-β and pro-fibrotic gene expression in γδ T cells. Conclusion: Within the IL-21-rich microenvironment of IgG4-RD, peripheral Vδ2 T cells acquire a Th2-like phenotype via the IL-21-STAT3-Blimp-1-GATA3 pathway. Targeting JAK/STAT3 inhibitors holds therapeutic potential for IgG4-RD.

Indexed as

Cell DifferentiationImmunoglobulin G4-Related DiseasePlasma CellsReceptors, Antigen, T-Cell, gamma-deltaTh2 CellsAgedCytokinesFemaleFibrosisGATA3 Transcription FactorHumansInterleukin-21InterleukinsLymphocyte ActivationMaleMiddle AgedCytokinesGATA3 Transcription FactorInterleukin-21InterleukinsReceptors, Antigen, T-Cell, gamma-deltaIgG4-related diseaseIL-21–STAT3plasmablastsTh2-like phenotypeVδ2 T cells

Identifiers

PMID40213561
PMCPMC11983612

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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.