Evidence map›Paper›PMID 26407164›Full record

ArticleImmunology2015

Inhibition of interleukin-1β-mediated interleukin-1 receptor-associated kinase 4 phosphorylation by zinc leads to repression of memory T helper type 17 response in humans.

Hyunju Lee, Bonah Kim, Yeon Ho Choi, Yuri Hwang, Dong Hyun Kim, Sunjung Cho, Sung Jun Hong, Won-Woo Lee

Open access · bronzeAbstract read
In one paragraph

Article in Immunology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers, 2 of them syntheses that pooled it.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed, 2 pooled it
1.2field-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

15 citing papers in PubMed, 2 syntheses or guidelines pooled it, 22 citations in OpenAlex.

  1. Pooled it
  2. Pooled it
  3. Review
  4. The roles of essential trace elements in T cell biology.Journal of cellular and molecular medicine · 2024
    Review
  5. Article
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  8. Article
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  13. Article
  14. Zinc and Sepsis.Nutrients · 2018
    Review
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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 3 countries.

Hyunju LeeDepartment of Microbiology and Immunology, Seoul National University College of Medicine, Seoul.
Bonah KimBK21Plus Biomedical Science Project, Seoul National University College of Medicine, Seoul.
Yeon Ho ChoiDepartment of Microbiology and Immunology, Seoul National University College of Medicine, Seoul.
Yuri HwangDepartment of Microbiology and Immunology, Seoul National University College of Medicine, Seoul.
Dong Hyun KimBK21Plus Biomedical Science Project, Seoul National University College of Medicine, Seoul.
Sunjung ChoDepartment of Microbiology and Immunology, Seoul National University College of Medicine, Seoul.
Sung Jun HongDepartment of Microbiology and Immunology, Seoul National University College of Medicine, Seoul.
Won-Woo LeeDepartment of Microbiology and Immunology, Seoul National University College of Medicine, Seoul.
New Generation University College · ETSeoul National University · KRNational University College · PR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Zinc is an essential trace element that plays pivotal roles in multiple facets of the immune system. Besides its catalytic and structural roles, zinc also functions as an intracellular signalling molecule, and changes in zinc levels can cause both direct and indirect modulation of immune responses. Further, cytoplasmic levels of bioavailable zinc in immune cells are largely influenced by many extracellular stimuli. Here we provide evidence that zinc represses memory T helper type 17 responses in humans by inhibiting interleukin-1β (IL-1β)-mediated signal. In vitro zinc treatment of CD4(+) T cells in the presence of activated monocytes inhibited interferon-γ-producing cells and IL-17-producing cells, but not IL-4-producing cells. Of note, production of IL-17(+) cells from memory CD4(+) T cells, which is significantly up-regulated by lipopolysaccharide-stimulated monocytes, was preferentially repressed by zinc. Increased cytoplasmic zinc in T cells suppressed IL-1β signalling through repression of phosphorylation of IL-1 receptor-associated kinase 4 (IRAK4), so leading to an inhibitory effect on T helper type 17 responses facilitated by monocyte-derived IL-1β in humans. These findings suggest that extracellular zinc bioavailability may affect memory CD4(+) T-cell responses by modulating the zinc-mediated signalling pathway.

Indexed as

Immunologic MemoryCD4-Positive T-LymphocytesCells, CulturedCytokinesHumansInterleukin-1betaInterleukin-1 Receptor-Associated KinasesLymphocyte ActivationModels, BiologicalMonocytesPhosphorylationSignal TransductionTh17 CellsZincCytokinesInterleukin-1betaInterleukin-1 Receptor-Associated KinasesZincinterleukin-1 receptor-associated kinase 4interleukin-1βmonocytesT helper type 17zinc

Identifiers

PMID26407164
PMCPMC4693897
OpenAlexW2146041221

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.