Evidence map›Paper›PMID 31405974›Full record

ArticleProceedings of the National Academy of Sciences of the United States of America2019

IL-17 constrains natural killer cell activity by restraining IL-15-driven cell maturation via SOCS3.

Xuefu Wang, Rui Sun, Xiaolei Hao, Zhe-Xiong Lian, Haiming Wei, Zhigang Tian

Open access · bronzeAbstract read
In one paragraph

Article in Proceedings of the National Academy of Sciences of the United States of America, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
1.8field-weighted citation impact, top 14% 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

28 citing papers in PubMed, 41 citations in OpenAlex.

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  10. Natural killer cells in the lung: potential role in asthma and virus-induced exacerbation?European respiratory review : an official journal of the European Respiratory Society · 2023
    Review
  11. Review
  12. T cells in health and disease.Signal transduction and targeted therapy · 2023
    Review
  13. Article
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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

6 authors at 3 institutions in 1 country.

Xuefu WangDivision of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, the Chinese Academy of Sciences (CAS) Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, 230027 Anhui, China.
Rui SunDivision of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, the Chinese Academy of Sciences (CAS) Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, 230027 Anhui, China.
Xiaolei HaoDivision of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, the Chinese Academy of Sciences (CAS) Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, 230027 Anhui, China.
Zhe-Xiong LianDivision of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, the Chinese Academy of Sciences (CAS) Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, 230027 Anhui, China.
Haiming WeiDivision of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, the Chinese Academy of Sciences (CAS) Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, 230027 Anhui, China.
Zhigang TianDivision of Molecular Medicine, Hefei National Laboratory for Physical Sciences at Microscale, the Chinese Academy of Sciences (CAS) Key Laboratory of Innate Immunity and Chronic Disease, School of Life Sciences, University of Science and Technology of China, Hefei, 230027 Anhui, China; tzg@ustc.edu.cn.
Chinese Academy of Sciences · CNAnhui Medical University · CNUniversity of Science and Technology of China · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Increasing evidence demonstrates that IL-17A promotes tumorigenesis, metastasis, and viral infection. Natural killer (NK) cells are critical for defending against tumors and infections. However, the roles and mechanisms of IL-17A in regulating NK cell activity remain elusive. Herein, our study demonstrated that IL-17A constrained NK cell antitumor and antiviral activity by restraining NK cell maturation. It was observed that the development and metastasis of tumors were suppressed in IL-17A-deficient mice in the NK cell-dependent manner. In addition, the antiviral activity of NK cells was also improved in IL-17A-deficient mice. Mechanistically, ablation of IL-17A signaling promoted generation of terminally mature CD27

Indexed as

AnimalsCell DifferentiationCytotoxicity, ImmunologicInterleukin-15Interleukin-17Killer Cells, NaturalLymphocyte ActivationMaleMelanoma, ExperimentalMiceMice, KnockoutSignal TransductionSuppressor of Cytokine Signaling 3 ProteinInterleukin-15Interleukin-17Suppressor of Cytokine Signaling 3 ProteinIL-15IL-17ANK cellsSOCS3terminal maturation

Identifiers

PMID31405974
PMCPMC6717263
OpenAlexW2967847451

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.