Evidence map›Paper›PMID 23555662›Full record

ArticlePloS one2013

Tissue inhibitor of metalloproteinase 1 is preferentially expressed in Th1 and Th17 T-helper cell subsets and is a direct STAT target gene.

Adewole Adamson, Kamran Ghoreschi, Matthew Rittler, Qian Chen, Hong-Wei Sun, Golnaz Vahedi, Yuka Kanno, William G Stetler-Stevenson, John J O'Shea, Arian Laurence

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.

0numbers the graph read from it
0cells of the map it votes in
14citing papers in PubMed
1.3field-weighted citation impact, top 21% 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

14 citing papers in PubMed, 23 citations in OpenAlex.

  1. Shared genetic association between inflammatory bowel disease and acute myeloid leukemia: insights from mendelian randomization and transcriptomic analyses.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2025
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  7. Investigation on the Mechanism of Qubi Formula in Treating Psoriasis Based on Network Pharmacology.Evidence-based complementary and alternative medicine : eCAM · 2020
    Article
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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

10 authors at 4 institutions in 3 countries.

Adewole AdamsonMolecular Immunology and Inflammation Branch, National Institute of Arthritis, Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD, USA.
Kamran Ghoreschi
Matthew Rittler
Qian Chen
Hong-Wei Sun
Golnaz Vahedi
Yuka Kanno
William G Stetler-Stevenson
John J O'Shea
Arian Laurence
National Institute of Arthritis and Musculoskeletal and Skin Diseases · USNational Cancer Institute · USHuazhong University of Science and Technology · CNNational Institutes of Health · US

Funding

Stat transcription factors in immunoregulation and autoimmune diseaseZIAAR041159 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI O'SHEA, JOHN · 2009 to 2025
$49.3M
Applying Bioinformatics to Research in Immune, Muscle, and Bone DiseasesZIHAR041173 · NIAMS · NATIONAL INSTITUTE OF ARTHRITIS AND MUSCULOSKELETAL AND SKIN DISEASES · PI GADINA, MASSIMO · 2009 to 2020
$11.0M
The Role of TIMPs in Cell Growth, Tumor Progression and MetastasisZIASC009179 · NCI · DIVISION OF CLINICAL SCIENCES - NCI · PI STETLER-STEVENSON, WILLIAM · 2009 to 2024
$9.7M
Intramural NIH HHS
6 · The paper itself

Abstract

CD4(+) T helper (Th) cells differentiate into distinct effector subsets that are critical for host defense, but are also implicated in the pathogenesis of autoimmune disorders. Thelper17 (Th17) cells in particular are emerging as important drivers of multiple diseases including psoriasis, spondyloarthropathy and multiple sclerosis. To gain insight into the function of Th17 cells, we performed transcriptional profiling in hopes of elucidating products not previously recognized as being functionally relevant in these T cells. Herein, we demonstrate that tissue inhibitor of metalloproteinase 1 (TIMP1), a secreted protein with pleiotropic effects on cellular growth, survival and integrity of the extracellular matrix, is preferentially produced by Th17 and Th1 cells. We further show that Th1 and Th17 cell TIMP1 regulation follows separate mechanisms with a requirement for STAT4 in the former and STAT3 in the latter. Finally, we demonstrate that when restricted to T cells, expression of TIMP1 promotes neuropathology in experimental allergic encephalomyelitis.

Indexed as

AnimalsCytokinesEncephalomyelitis, Autoimmune, ExperimentalGene Expression ProfilingGene Expression RegulationHumansMiceMice, TransgenicOrgan SpecificitySignal TransductionSpleenSTAT3 Transcription FactorSTAT4 Transcription FactorTh17 CellsTh1 CellsTissue Inhibitor of Metalloproteinase-1CytokinesStat3 protein, mouseSTAT3 Transcription FactorStat4 protein, mouseSTAT4 Transcription FactorTimp1 protein, mouseTissue Inhibitor of Metalloproteinase-1

Identifiers

PMID23555662
PMCPMC3608653
OpenAlexW2017551282

What OpenQuestion holds

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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.