Evidence map›Paper›PMID 33185980›Full record

ArticleJournal of cellular and molecular medicine2020

Chronic shift-lag promotes NK cell ageing and impairs immunosurveillance in mice by decreasing the expression of CD122.

Xiaokang Zeng, Caiying Liang, Jie Yao

Open access · goldAbstract read
In one paragraph

Article in Journal of cellular and molecular medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 29 papers.

0numbers the graph read from it
0cells of the map it votes in
29citing papers in PubMed
1.0field-weighted citation impact, top 28% 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

29 citing papers in PubMed, 31 citations in OpenAlex.

  1. Arntl deficiency impairs NK cell function by reducing responsiveness to IL-15 and suppressing activation.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2026
    Article
  2. Circadian rhythms and lung cancer biology and immunotherapy: Emerging opportunities and challenges.Chinese medical journal pulmonary and critical care medicine · 2026
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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

3 authors at 2 institutions in 1 country.

Xiaokang ZengMedical Research Center and Department of Laboratory Medicine, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde, Foshan), Foshan, China.ORCID 0000-0002-6531-2502
Caiying LiangGuangdong Keyway Testing Technology Co, Ltd., Foshan, China.ORCID 0000-0001-8742-0515
Jie YaoMedical Research Center and Department of Laboratory Medicine, Shunde Hospital, Southern Medical University (The First People's Hospital of Shunde, Foshan), Foshan, China.ORCID 0000-0002-8935-0722
The First People's Hospital of Shunde · CNChina Guangzhou Analysis and Testing Center · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Long-term subjection to shift work increases the risk of cancer. The purpose of the present study was to explore the mechanism by which chronic circadian disruption impairs natural killer (NK) cell immunosurveillance. Mice were subjected to light-dark reverse every 4 days for 12 weeks to disrupt normal circadian rhythm. NK cell development and function were evaluated by flow cytometry. The mRNA and protein levels of period 1 (per1) and per2 were suppressed, while circadian locomotor output cycle kaput (CLOCK) was increased in the shifted mice, indicating successful generation of the circadian rhythm disruption mouse model. Chronic shift-lag promoted NK cell ageing, which is likely due to the reduction in Ly49 family receptor expression in shifted NK. We further studied the effects of circadian rhythm disruption on NK cell function. Chronic shift-lag inhibited NK cell secretion of granular CD107a and interferon gamma. Moreover, chronic shift-lag attenuated the clearance of MHC-I-deficient tumour cells by NK cells in vivo and promoted lung metastasis of B16F10 melanomas. Furthermore, chronic shift-lag reduced NK cell killing function, which may be due to the suppression of Eomes transcription factor expression, which inhibiting the transcription of CD122. In conclusion, our findings suggest that chronic circadian disruption attenuates NK cell cytolytic activity by decreasing the expression of CD122.

Indexed as

Cellular SenescenceImmunologic SurveillanceAnimalsApoptosisBiomarkersCell ProliferationCircadian RhythmGene Expression RegulationInterferon-gammaInterleukin-2 Receptor beta SubunitKiller Cells, NaturalLysosomal-Associated Membrane Protein 1Lysosomal Membrane ProteinsMaleMiceShift Work ScheduleBiomarkersIl2rb protein, mouseInterferon-gammaInterleukin-2 Receptor beta SubunitLamp1 protein, mouseLysosomal-Associated Membrane Protein 1Lysosomal Membrane ProteinsCD122circadian rhythm disruptionEomesNK cell developmentNK cell function

Identifiers

PMID33185980
PMCPMC7754032
OpenAlexW3103848734

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.