Evidence map›Paper›PMID 26479789›Full record

ArticleNature immunology2015

The phosphatase DUSP2 controls the activity of the transcription activator STAT3 and regulates TH17 differentiation.

Dan Lu, Liang Liu, Xin Ji, Yanan Gao, Xi Chen, Yu Liu, Yang Liu, Xuyang Zhao, Yan Li, Yunqiao Li and 4 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 96 papers.

0numbers the graph read from it
0cells of the map it votes in
96citing papers in PubMed
3.3field-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

96 citing papers in PubMed, 154 citations in OpenAlex.

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  16. Protein phosphatases in systemic autoimmunity.Immunometabolism (Cobham, Surrey) · 2025
    Review
  17. Review
  18. Article
  19. Review
  20. Review

36 more citing papers are in PubMed but not listed here.

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

14 authors at 1 institution in 1 country.

Dan LuInstitute of Systems Biomedicine, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Liang LiuInstitute of Systems Biomedicine, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Xin JiInstitute of Systems Biomedicine, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Yanan GaoDepartment of Immunology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Xi ChenInstitute of Systems Biomedicine, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Yu LiuInstitute of Systems Biomedicine, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Yang LiuInstitute of Systems Biomedicine, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Xuyang ZhaoInstitute of Systems Biomedicine, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Yan LiDepartment of Immunology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Yunqiao LiInstitute of Systems Biomedicine, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Yan JinInstitute of Systems Biomedicine, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Yu ZhangDepartment of Immunology, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Michael A McNuttInstitute of Systems Biomedicine, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Yuxin YinInstitute of Systems Biomedicine, School of Basic Medical Sciences, Peking University Health Science Center, Beijing, China.
Peking University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Deregulation of the TH17 subset of helper T cells is closely linked with immunological disorders and inflammatory diseases. However, the mechanism by which TH17 cells are regulated remains elusive. Here we found that the phosphatase DUSP2 (PAC1) negatively regulated the development of TH17 cells. DUSP2 was directly associated with the signal transducer and transcription activator STAT3 and attenuated its activity through dephosphorylation of STAT3 at Tyr705 and Ser727. DUSP2-deficient mice exhibited severe susceptibility to experimental colitis, with enhanced differentiation of TH17 cells and secretion of proinflammatory cytokines. In clinical patients with ulcerative colitis, DUSP2 was downregulated by DNA methylation and was not induced during T cell activation. Our data demonstrate that DUSP2 is a true STAT3 phosphatase that modulates the development of TH17 cells in the autoimmune response and inflammation.

Indexed as

AnimalsCell DifferentiationCells, CulturedColitisColitis, UlcerativeCytokinesDextran SulfateDNA MethylationDual Specificity Phosphatase 2Gene Expression RegulationHEK293 CellsHumansImmunoblottingInflammation MediatorsMice, Inbred C57BLMice, KnockoutCytokinesDextran SulfateDual Specificity Phosphatase 2Dusp2 protein, mouseInflammation MediatorsSTAT3 Transcription FactorTyrosine

Identifiers

PMID26479789
OpenAlexW1777296950

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.