Evidence map›Paper›PMID 28585539›Full record

ArticleNature communications2017

IL-21-mediated reversal of NK cell exhaustion facilitates anti-tumour immunity in MHC class I-deficient tumours.

Hyungseok Seo, Insu Jeon, Byung-Seok Kim, Myunghwan Park, Eun-Ah Bae, Boyeong Song, Choong-Hyun Koh, Kwang-Soo Shin, Il-Kyu Kim, Kiyoung Choi and 8 more

Open access · goldAbstract read
In one paragraph

Article in Nature communications, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 105 papers.

0numbers the graph read from it
0cells of the map it votes in
105citing papers in PubMed
6.6field-weighted citation impact, top 2% 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

105 citing papers in PubMed, 156 citations in OpenAlex.

  1. Trial
  2. CD4Cell death & disease · 2022
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  13. LAG3 Marks Activated but Hyporesponsive NK Cells.European journal of immunology · 2025
    Article
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  15. Article
  16. Article
  17. Frontiers in genetics · 2025
    Article
  18. Review
  19. Review
  20. Article

45 more citing papers are in PubMed but not listed here.

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

18 authors at 5 institutions in 2 countries.

Hyungseok SeoLaboratory of Immunology, Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul 08826, Republic of Korea.
Insu JeonLaboratory of Immunology, Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul 08826, Republic of Korea.
Byung-Seok KimLaboratory of Immune Regulation, Research Institute of Pharmaceutical Science, College of Pharmacy, Seoul National University, Seoul 08826, Republic of Korea.
Myunghwan ParkLaboratory of Immunology, Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul 08826, Republic of Korea.
Eun-Ah BaeLaboratory of Immunology, Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul 08826, Republic of Korea.ORCID 0000-0002-9413-2543
Boyeong SongLaboratory of Immunology, Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul 08826, Republic of Korea.
Choong-Hyun KohLaboratory of Immunology, Research Institute of Pharmaceutical Science, College of Pharmacy Seoul National University, Seoul 08826, Republic of Korea.
Kwang-Soo ShinLaboratory of Immunology, Research Institute of Pharmaceutical Science, College of Pharmacy Seoul National University, Seoul 08826, Republic of Korea.
Il-Kyu KimLaboratory of Immunology, Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul 08826, Republic of Korea.ORCID 0000-0002-4661-0133
Kiyoung ChoiCellid, Inc., Seoul 08826, Republic of Korea.
Taegwon OhCellid, Inc., Seoul 08826, Republic of Korea.
Jiyoun MinDepartment of Biological Science, Korea Advanced Institute of Science and Technology, Daejeon 34141, Republic of Korea.
Byung Soh MinDepartment of Surgery, Yonsei University College of Medicine, Seoul 03722, Republic of Korea.
Yoon Dae HanDepartment of Surgery, Yonsei University College of Medicine, Seoul 03722, Republic of Korea.
Suk-Jo KangDepartment of Biological Science, Korea Advanced Institute of Science and Technology, Daejeon 34141, Republic of Korea.
Sang Joon ShinDepartment of Internal Medicine, Yonsei University College of Medicine, Seoul 03722, Republic of Korea.
Yeonseok ChungLaboratory of Immune Regulation, Research Institute of Pharmaceutical Science, College of Pharmacy, Seoul National University, Seoul 08826, Republic of Korea.ORCID 0000-0001-5780-4841
Chang-Yuil KangLaboratory of Immunology, Department of Molecular Medicine and Biopharmaceutical Sciences, Graduate School of Convergence Science and Technology, Seoul National University, Seoul 08826, Republic of Korea.ORCID 0000-0002-1843-6967
Seoul National University of Science and Technology · KRSeoul National University · KRYonsei University · KRCellid (South Korea) · KRKorea Advanced Institute of Science and Technology · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

During cancer immunoediting, loss of major histocompatibility complex class I (MHC-I) in neoplasm contributes to the evasion of tumours from host immune system. Recent studies have demonstrated that most natural killer (NK) cells that are found in advanced cancers are defective, releasing the malignant MHC-I-deficient tumours from NK-cell-dependent immune control. Here, we show that a natural killer T (NKT)-cell-ligand-loaded tumour-antigen expressing antigen-presenting cell (APC)-based vaccine effectively eradicates these advanced tumours. During this process, we find that the co-expression of Tim-3 and PD-1 marks functionally exhausted NK cells in advanced tumours and that MHC-I downregulation in tumours is closely associated with the induction of NK-cell exhaustion in both tumour-bearing mice and cancer patients. Furthermore, the recovery of NK-cell function by IL-21 is critical for the anti-tumour effects of the vaccine against advanced tumours. These results reveal the process involved in the induction of NK-cell dysfunction in advanced cancers and provide a guidance for the development of strategies for cancer immunotherapy.

Indexed as

Genes, MHC Class IAnimalsBiomarkers, TumorCancer VaccinesColorectal NeoplasmsHepatitis A Virus Cellular Receptor 2HumansInterleukin-21InterleukinsKiller Cells, NaturalMelanomaMice, Inbred BALB CMice, Inbred C57BLProgrammed Cell Death 1 ReceptorUrinary Bladder NeoplasmsXenograft Model Antitumor AssaysBiomarkers, TumorCancer VaccinesHAVCR2 protein, humanHepatitis A Virus Cellular Receptor 2Interleukin-21InterleukinsPDCD1 protein, humanProgrammed Cell Death 1 Receptor

Identifiers

PMID28585539
PMCPMC5467212
OpenAlexW2621506639

What OpenQuestion holds

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LicenceCC BY
Read underepoch 390

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.