Evidence map›Paper›PMID 29163491›Full record

ArticleFrontiers in immunology2017

Suppression of Natural Killer Cell Activity by Regulatory NKT10 Cells Aggravates Alcoholic Hepatosteatosis.

Kele Cui, Guoxiu Yan, Xiaodong Zheng, Li Bai, Haiming Wei, Rui Sun, Zhigang Tian

Open access · goldAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Frontiers in immunology, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.

0numbers the graph read from it
0cells of the map it votes in
16citing papers in PubMed
0.8field-weighted citation impact, top 29% 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

16 citing papers in PubMed, 27 citations in OpenAlex.

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  9. Food science & nutrition · 2021
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  16. Pathogenesis of Alcohol-Associated Liver Disease.Journal of clinical and experimental hepatology
    Review
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

7 authors at 4 institutions in 1 country.

Kele CuiThe CAS Key Laboratory of Innate Immunity and Chronic Disease and Institute of Immunology, School of Life Sciences and Medical Center, University of Science & Technology of China, Hefei, China.
Guoxiu YanThe CAS Key Laboratory of Innate Immunity and Chronic Disease and Institute of Immunology, School of Life Sciences and Medical Center, University of Science & Technology of China, Hefei, China.
Xiaodong ZhengThe CAS Key Laboratory of Innate Immunity and Chronic Disease and Institute of Immunology, School of Life Sciences and Medical Center, University of Science & Technology of China, Hefei, China.
Li BaiThe CAS Key Laboratory of Innate Immunity and Chronic Disease and Institute of Immunology, School of Life Sciences and Medical Center, University of Science & Technology of China, Hefei, China.
Haiming WeiThe CAS Key Laboratory of Innate Immunity and Chronic Disease and Institute of Immunology, School of Life Sciences and Medical Center, University of Science & Technology of China, Hefei, China.
Rui SunThe CAS Key Laboratory of Innate Immunity and Chronic Disease and Institute of Immunology, School of Life Sciences and Medical Center, University of Science & Technology of China, Hefei, China.
Zhigang TianThe CAS Key Laboratory of Innate Immunity and Chronic Disease and Institute of Immunology, School of Life Sciences and Medical Center, University of Science & Technology of China, Hefei, China.
University of Science and Technology of China · CNAnhui Medical University · CNState Key Laboratory of Diagnosis and Treatment of Infectious DiseasesZhejiang University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

We and others have found that the functions of hepatic natural killer (NK) cells are inhibited but invariant NKT (iNKT) cells become activated after alcohol drinking, leaving a possibility that there exists interplay between NK cells and iNKT cells during alcoholic liver disease. Here, in a chronic plus single-binge ethanol consumption mouse model, we observed that NK cells and interferon-γ (IFN-γ) protected against ethanol-induced liver steatosis, as both wild-type (WT) mice treated with anti-asialo GM1 antibody and IFN-γ-deficient GKO mice developed more severe alcoholic fatty livers. As expected, IFN-γ could directly downregulate lipogenesis in primary hepatocytes

Indexed as

alcoholic fatty liverinteractioninterferon-γinterleukin-10invariant natural killer T cellsnatural killer cells

Identifiers

PMID29163491
PMCPMC5670109
OpenAlexW2765826911

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.