Evidence map›Paper›PMID 24498194›Full record

ArticlePloS one2014

The modulation of endoplasmic reticulum stress by chemical chaperone upregulates immune negative cytokine IL-35 in apolipoprotein E-deficient mice.

Bo Wang, Shen Dai, Zhaojing Dong, Yue Sun, Xingguo Song, Chun Guo, Faliang Zhu, Qun Wang, Lining Zhang

Open access · goldAbstract read
In one paragraph

Article in PloS one, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.

0numbers the graph read from it
0cells of the map it votes in
13citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

13 citing papers in PubMed, 23 citations in OpenAlex.

  1. Article
  2. Article
  3. Article
  4. Interleukin-35: Structure, Function and Its Impact on Immune-Related Diseases.Journal of interferon & cytokine research : the official journal of the International Society for Interferon and Cytokine Research · 2021
    Review
  5. Review
  6. Review
  7. Targeting IRE1 with small molecules counteracts progression of atherosclerosis.Proceedings of the National Academy of Sciences of the United States of America · 2017
    Article
  8. Article
  9. Article
  10. IL-35 improves TExperimental and therapeutic medicine · 2016
    Article
  11. Article
  12. Review
  13. Article
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

9 authors at 1 institution in 1 country.

Bo WangDepartment of Immunology, Shandong University School of Medicine, Jinan, Shandong, China.
Shen DaiDepartment of Immunology, Shandong University School of Medicine, Jinan, Shandong, China.
Zhaojing DongDepartment of Immunology, Shandong University School of Medicine, Jinan, Shandong, China.
Yue SunDepartment of Immunology, Shandong University School of Medicine, Jinan, Shandong, China.
Xingguo SongDepartment of Immunology, Shandong University School of Medicine, Jinan, Shandong, China.
Chun GuoDepartment of Immunology, Shandong University School of Medicine, Jinan, Shandong, China.
Faliang ZhuDepartment of Immunology, Shandong University School of Medicine, Jinan, Shandong, China.
Qun WangDepartment of Immunology, Shandong University School of Medicine, Jinan, Shandong, China.
Lining ZhangDepartment of Immunology, Shandong University School of Medicine, Jinan, Shandong, China.
Shandong University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Interleukin (IL)-35 is a newly identified immune negative molecule which is secreted by CD4(+)Foxp3(+) T regulatory cells (Tregs) and contributes to their suppressive capacity. Early data have shown that IL-35 inhibits development of several autoimmune diseases. However, the role of IL-35 in atherosclerosis, a lipid-driven chronic inflammatory disease in arterial wall, remains to be investigated. Here, we found that IL-35 was involved in atherosclerosis in apolipoprotein E-deficient (ApoE(-/-)) mice. ApoE(-/-) mice with established atherosclerotic lesion displayed a lower level of IL-35 compared to age-matched wild type C57BL/6 mice without plaque. However, IL-35 expression increased significantly in ApoE(-/-) mice with attenuated plaque. More importantly, we found that modulation of ER stress treated by chemical chaperone, 4-Phenyl butyric acid (PBA) in vivo, mainly upregulated immune negative regulating molecule IL-35, as well as IL-10 and Foxp3, accompanied by increased Tregs. However, no obvious impact on pro-inflammatory molecules such as TNF-α, IFN-γ, IL-17 and IL-23 was observed, which provides new insight into the benefit of ER stress recovery from attenuated plaque. Our results suggest that IL-35 might have a potential value for atherosclerotic therapy.

Indexed as

AnimalsApolipoproteins EAtherosclerosisDisease Models, AnimalEndoplasmic Reticulum StressForkhead Transcription FactorsInterferon-gammaInterleukinsMaleMiceMice, Inbred C57BLPlaque, AtheroscleroticTumor Necrosis Factor-alphaUp-RegulationApolipoproteins EForkhead Transcription FactorsFoxp3 protein, mouseInterferon-gammainterleukin-35, mouseInterleukinsTumor Necrosis Factor-alpha

Identifiers

PMID24498194
PMCPMC3907489
OpenAlexW2030534532

What OpenQuestion holds

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LicenceCC BY
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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.