Evidence map›Paper›PMID 26507712›Full record

ArticleNature communications2015

Ndrg1 is a T-cell clonal anergy factor negatively regulated by CD28 costimulation and interleukin-2.

Yu Mi Oh, Hyung Bae Park, Jae Hun Shin, Ji Eun Lee, Ha Young Park, Dhong Hyo Kho, Jun Sung Lee, Heonsik Choi, Tomohiko Okuda, Koichi Kokame and 5 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 26 papers.

0numbers the graph read from it
0cells of the map it votes in
26citing papers in PubMed
2.2field-weighted citation impact, top 13% 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

26 citing papers in PubMed, 35 citations in OpenAlex.

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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

15 authors at 5 institutions in 3 countries.

Yu Mi OhDepartment of Biochemistry and Molecular Biology, Seoul National University College of Medicine, 103 Daehak-ro, Chongno-gu, Seoul 110-799, Korea.
Hyung Bae ParkDepartment of Biochemistry and Molecular Biology, Seoul National University College of Medicine, 103 Daehak-ro, Chongno-gu, Seoul 110-799, Korea.
Jae Hun ShinSpecific Organs Cancer Branch, Research Institute National Cancer Center, Gyeonggi-do 410-769, Korea.
Ji Eun LeeDepartment of Biochemistry and Molecular Biology, Seoul National University College of Medicine, 103 Daehak-ro, Chongno-gu, Seoul 110-799, Korea.
Ha Young ParkDepartment of Biochemistry and Molecular Biology, Seoul National University College of Medicine, 103 Daehak-ro, Chongno-gu, Seoul 110-799, Korea.
Dhong Hyo KhoSpecific Organs Cancer Branch, Research Institute National Cancer Center, Gyeonggi-do 410-769, Korea.
Jun Sung LeeSpecific Organs Cancer Branch, Research Institute National Cancer Center, Gyeonggi-do 410-769, Korea.
Heonsik ChoiLaboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
Tomohiko OkudaDepartment of Molecular Pathogenesis, National Cerebral and Cardiovascular Center, Suita, Osaka 565-8565, Japan.
Koichi KokameDepartment of Molecular Pathogenesis, National Cerebral and Cardiovascular Center, Suita, Osaka 565-8565, Japan.
Toshiyuki MiyataDepartment of Molecular Pathogenesis, National Cerebral and Cardiovascular Center, Suita, Osaka 565-8565, Japan.
In-Hoo KimMolecular Imaging and Therapy Branch, Research Institute National Cancer Center, Gyeonggi-do 410-769, Korea.
Seung Hoon LeeSpecific Organs Cancer Branch, Research Institute National Cancer Center, Gyeonggi-do 410-769, Korea.
Ronald H SchwartzLaboratory of Cellular and Molecular Immunology, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, Maryland 20892, USA.
Kyungho ChoiDepartment of Biochemistry and Molecular Biology, Seoul National University College of Medicine, 103 Daehak-ro, Chongno-gu, Seoul 110-799, Korea.
National Cancer Center · KRSeoul National University · KRNational Cerebral and Cardiovascular Center · JPNational Institute of Allergy and Infectious Diseases · USNational Institutes of Health · US

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Induction of T-cell clonal anergy involves serial activation of transcription factors, including NFAT and Egr2/3. However, downstream effector mechanisms of these transcription factors are not fully understood yet. Here we identify Ndrg1 as an anergy factor induced by Egr2. Ndrg1 is upregulated by anergic signalling and maintained at high levels in resting anergic T cells. Overexpression of Ndrg1 mimics the anergic state and knockout of the gene prevents anergy induction. Interestingly, Ndrg1 is phosphorylated and degraded by CD28 signalling in a proteasome-dependent manner, explaining the costimulation dependence of anergy prevention. Similarly, IL-2 treatment of anergic T cells, under conditions that lead to the reversal of anergy, also induces Ndrg1 phosphorylation and degradation. Finally, older Ndrg1-deficient mice show T-cell hyperresponsiveness and Ndrg1-deficient T cells aggravate inducible autoimmune inflammation. Thus, Ndrg1 contributes to the maintenance of clonal anergy and inhibition of T-cell-mediated inflammation.

Indexed as

Clonal AnergyDown-RegulationAnimalsCD28 AntigensCell Cycle ProteinsEarly Growth Response Protein 2Interleukin-2Intracellular Signaling Peptides and ProteinsLymphocyte ActivationMiceMice, Inbred C57BLMice, KnockoutN-myc Downstream-Regulated Gene 1 ProteinT-LymphocytesCD28 AntigensCell Cycle ProteinsEarly Growth Response Protein 2Egr2 protein, mouseInterleukin-2Intracellular Signaling Peptides and ProteinsN-myc Downstream-Regulated Gene 1 Protein

Identifiers

PMID26507712
PMCPMC4846325
OpenAlexW2258382678

What OpenQuestion holds

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LicenceCC BY
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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.