Evidence map›Paper›PMID 34335571›Full record

ArticleFrontiers in immunology2021

IL-33 Drives Expansion of Type 2 Innate Lymphoid Cells and Regulatory T Cells and Protects Mice From Severe, Acute Colitis.

Nhi Ngo Thi Phuong, Vittoria Palmieri, Alexandra Adamczyk, Robert Klopfleisch, Jost Langhorst, Wiebke Hansen, Astrid M Westendorf, Eva Pastille

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.5field-weighted citation impact, top 6% 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

42 citing papers in PubMed, 54 citations in OpenAlex.

  1. Article
  2. Elevated ST2Arthritis research & therapy · 2026
    Article
  3. [Effect of interleukin-33 on glucocorticoid-induced osteonecrosis of the femoral head in mice].Zhongguo xiu fu chong jian wai ke za zhi = Zhongguo xiufu chongjian waike zazhi = Chinese journal of reparative and reconstructive surgery · 2026
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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

8 authors at 3 institutions in 1 country.

Nhi Ngo Thi PhuongInstitute of Medical Microbiology, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
Vittoria PalmieriInstitute of Medical Microbiology, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
Alexandra AdamczykInstitute of Medical Microbiology, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
Robert KlopfleischInstitute of Veterinary Pathology, Freie Universitaet Berlin, Berlin, Germany.
Jost LanghorstDepartment of Internal and Integrative Medicine, Klinikum Bamberg, Chair for Integrative Medicine, University of Duisburg-Essen, Bamberg, Germany.
Wiebke HansenInstitute of Medical Microbiology, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
Astrid M WestendorfInstitute of Medical Microbiology, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
Eva PastilleInstitute of Medical Microbiology, University Hospital Essen, University Duisburg-Essen, Essen, Germany.
University of Duisburg-Essen · DEFreie Universität Berlin · DESozialstiftung Bamberg · DE

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The hallmarks of inflammatory bowel disease are mucosal damage and ulceration, which are known to be high-risk conditions for the development of colorectal cancer. Recently, interleukin (IL)-33 and its receptor ST2 have emerged as critical modulators in inflammatory disorders. Even though several studies highlight the IL-33/ST2 pathway as a key factor in colitis, a detailed mode of action remains elusive. Therefore, we investigated the role of IL-33 during intestinal inflammation and its potential as a novel therapeutic target in colitis. Interestingly, the expression of IL-33, but not its receptor ST2, was significantly increased in biopsies from the inflamed colon of IBD patients compared to non-inflamed colonic tissue. Accordingly, in a mouse model of Dextran Sulfate Sodium (DSS) induced colitis, the secretion of IL-33 significantly accelerated in the colon. Induction of DSS colitis in

Indexed as

Adoptive TransferAnimalsAnti-Inflammatory AgentsCell ProliferationColitisColonDextran SulfateDisease Models, AnimalDNA-Binding ProteinsFemaleGoblet CellsHumansImmunity, InnateInterleukin-1 Receptor-Like 1 ProteinInterleukin-33Intestinal MucosaAnti-Inflammatory AgentsDextran SulfateDNA-Binding ProteinsIl1rl1 protein, mouseIl33 protein, mouseInterleukin-1 Receptor-Like 1 ProteinInterleukin-33Rag2 protein, mousecolitisIL-33ILC2intestinal inflammationST2Tregs

Identifiers

PMID34335571
PMCPMC8320374
OpenAlexW3185942960

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.