Evidence map›Paper›PMID 28690324›Full record

ArticleCellular & molecular immunology2017

Proteasome inhibition suppresses Th17 cell generation and ameliorates autoimmune development in experimental Sjögren's syndrome.

Fan Xiao, Xiang Lin, Jie Tian, Xiaohui Wang, Qian Chen, Ke Rui, Jie Ma, Shengjun Wang, Qingwen Wang, Xiaoqi Wang and 3 more

Open access · bronzeAbstract read
In one paragraph

Article in Cellular & molecular immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 34 papers.

0numbers the graph read from it
0cells of the map it votes in
34citing papers in PubMed
3.4field-weighted citation impact, top 7% 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

34 citing papers in PubMed, 60 citations in OpenAlex.

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  7. Proteasome: Role in T Cell Function Regulation.International journal of biological sciences · 2025
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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

13 authors at 5 institutions in 2 countries.

Fan XiaoDepartment of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong, Hong Kong, China.
Xiang LinDepartment of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong, Hong Kong, China.
Jie TianDepartment of Immunology, Jiangsu University Medical School, Zhenjiang, Jiangsu 212013 China.
Xiaohui WangDepartment of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong, Hong Kong, China.
Qian ChenDepartment of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong, Hong Kong, China.
Ke RuiDepartment of Immunology, Jiangsu University Medical School, Zhenjiang, Jiangsu 212013 China.
Jie MaDepartment of Immunology, Jiangsu University Medical School, Zhenjiang, Jiangsu 212013 China.
Shengjun WangDepartment of Immunology, Jiangsu University Medical School, Zhenjiang, Jiangsu 212013 China.
Qingwen WangDepartment of Rheumatology and Immunology, Peking University Shenzhen Hospital, Shenzhen, Guangdong 518036, China.
Xiaoqi WangDepartment of Rheumatology, Shenzhen People's Hospital, Shenzhen, Guangdong 518020, China.
Dongzhou LiuDepartment of Rheumatology, Shenzhen People's Hospital, Shenzhen, Guangdong 518020, China.
Lingyun SunDepartment of Rheumatology and Immunology, The Affiliated Drum Tower Hospital of Nanjing University Medical School, Nanjing, Jiangsu 210008, China.
Liwei LuDepartment of Pathology and Shenzhen Institute of Research and Innovation, The University of Hong Kong, Hong Kong, China.
City University of Hong Kong, Shenzhen Research Institute · CNJiangsu University · CNNanjing Drum Tower Hospital · CNPeking University Shenzhen Hospital · CNShenZhen People’s Hospital · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Immunoproteasome activation in immune cells is involved in the modulation of immune responses. Increasing evidence indicates that proteasome inhibitors show beneficial effects in treating autoimmune diseases, but it remains unclear whether proteasome inhibition is an effective approach for suppressing autoimmune development in Sjögren's syndrome (SS). Our previous work has demonstrated a critical role for Th17 cells in the development of experimental SS (ESS) in mice. In this study, we detected high levels of low-molecular-weight protein 7 (LMP7), a key subunit of the immunoproteasome, in Th17 cells from ESS mice. Moreover, treatment with bortezomib (BTZ), a proteasome inhibitor, markedly suppressed Th17 differentiation in both murine and human naive T cells in culture. Furthermore, ESS mice treated with BTZ displayed significantly higher saliva flow rates and a reduction in tissue destruction in the salivary glands compared with vehicle-treated ESS mice. Notably, BTZ-treated ESS mice showed markedly decreased Th17 cells, germinal center B cells and plasma cells in the peripheral lymphoid organs. In addition, adoptively transferred wild type naive CD4

Identifiers

PMID28690324
PMCPMC5675963
OpenAlexW2734717940

What OpenQuestion holds

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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.