Evidence map›Paper›PMID 36567407›Full record

ArticleClinical rheumatology2023

Immune phenotype changes in IgG4-related disease: CD161 + Treg and Foxp3 + Treg.

Wenjie Bian, Yingni Li, Feng Sun, Xiaolin Sun, Ru Li, Changsheng Xia, Jiangnan Fu, Yuxin Zhang, Shuang Chen, Yanying Liu

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Article in Clinical rheumatology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.0field-weighted citation impact, top 22% of its field
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

6 citing papers in PubMed, 7 citations in OpenAlex.

  1. Article
  2. Elevated Peripheral CD161ACR open rheumatology · 2026
    Article
  3. Article
  4. Review
  5. Article
  6. 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

10 authors at 2 institutions in 1 country.

Wenjie Bian *Department of Rheumatology and Immunology, Peking University People's Hospital, 11, Xizhimen South Street, Beijing, 100044, China.
Yingni Li *Department of Rheumatology and Immunology, Peking University People's Hospital, 11, Xizhimen South Street, Beijing, 100044, China.
Feng Sun *Department of Rheumatology and Immunology, Peking University People's Hospital, 11, Xizhimen South Street, Beijing, 100044, China.
Xiaolin SunDepartment of Rheumatology and Immunology, Peking University People's Hospital, 11, Xizhimen South Street, Beijing, 100044, China.
Ru LiDepartment of Rheumatology and Immunology, Peking University People's Hospital, 11, Xizhimen South Street, Beijing, 100044, China.
Changsheng XiaDepartment of Clinical Laboratory, Peking University People's Hospital, Beijing, 100044, China.
Jiangnan FuDepartment of Rheumatology and Immunology, Peking University People's Hospital, 11, Xizhimen South Street, Beijing, 100044, China.
Yuxin ZhangDepartment of Rheumatology and Immunology, Peking University People's Hospital, 11, Xizhimen South Street, Beijing, 100044, China.
Shuang ChenDepartment of Rheumatology and Immunology, Peking University People's Hospital, 11, Xizhimen South Street, Beijing, 100044, China.
Yanying LiuDepartment of Rheumatology and Immunology, Peking University People's Hospital, 11, Xizhimen South Street, Beijing, 100044, China. 57495011@qq.com.ORCID http://orcid.org/0000-0003-2609-4052
Peking University · CNCapital Medical University · CN

Funding

Capital's Funds for Health Improvement and Research 2022-2-2026National Natural Science Foundation of China U1903210
6 · The paper itself

Abstract

objectiveWe aimed to characterize the alterations in the immune phenotypes and explore the potential relevance to pathogenesis in IgG4-RD.

methodsForty-two IgG4-RD patients and thirty-eight healthy controls were recruited in this study. Peripheral immunocompetent cells including T cells, CD4 + T cells, CD8 + T cells, B cells, NK cells CD4 + CD45RA + T cells (naïve T cells), CD4 + CD25 - / + Foxp3 - T cells (Teff), CD4 + CD25hiCD127lowCD161 + T cells (CD161 + Treg), CD4 + CD25hiFoxp3 + T cells (Foxp3 + Treg), CD4 + CD4RA-CXCR5 + PD1 + CCR7low T cells (pTfh), T helper (Th) 1, Th2, and Th17 before and after treatment were immunophenotyped by flow cytometry.

resultsCompared with healthy controls, IgG4-RD patients showed higher proportions of NK (20.1% vs 13.6%, p < 0.01), Th1 (CD4 + IFN-γ + : 17.9% vs 14.2%, p = 0.061; TNF-α: 43.7% vs 36.7%, p < 0.05), Th2 (CD4 + IL-4 + : 2.4% vs 1.3%, p < 0.0001), CD161 + Treg (14.9% vs 11.6%, p < 0.01), pTfh (3.2% vs 2.4%, p < 0.05), and Foxp3 + Treg (8.3% vs 7.0%, p < 0.01) and lower proportions of B lymphocytes (8.4% vs 13.1%, p < 0.001), Teff (91.6% vs 92.6%, p < 0.01), and naïve Th cells (19.9% vs 32.1%, p < 0.01) before treatment. Foxp3 + Treg percentage decreased significantly after treatment (8.6% vs 6.9%, p < 0.05). Both serum C3 (r =  - 0.6374, p < 0.01) and C4 (r =  - 0.6174, p < 0.01) levels were in negative correlation with CD161 + Treg. The eosinophil percentage was positively correlated with Foxp3 + Treg (r = 0.5435, p < 0.05). Serum IgE level was positively correlated with Th2 (r = 0.5545, p < 0.05). There was a positive correlation between CD161 + Treg and pTfh (r = 0.4974, p < 0.05) while a negative correlation between Th2 and B cells (r =  - 0.4925, p < 0.05).

conclusionImmune phenotypes were altered in IgG4-RD. Treg/Teff balance was shifted toward Treg in IgG4-RD. CD161 + Treg was likely to be involved in the pathogenesis of IgG4-RD. Key Points •Immune phenotypes were altered in B cells, T cells, and NK cells in IgG4-RD. •Treg/Teff balance was shifted toward Treg in IgG4-RD. •CD161+ Treg maybe play a proinflammatory role in IgG4-RD.

Indexed as

Immunoglobulin G4-Related DiseaseT-Lymphocytes, RegulatoryCD4-Positive T-LymphocytesForkhead Transcription FactorsHumansPhenotypeTh17 CellsForkhead Transcription FactorsFOXP3 protein, humanCD161 + TregFoxp3 + TregIgG4-RDTreatment

Identifiers

PMID36567407
OpenAlexW4312196546

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Registered trials

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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.