Evidence map›Paper›PMID 36624164›Full record

ArticleNature immunology2023

NgR1 is an NK cell inhibitory receptor that destabilizes the immunological synapse.

Se-Chan Oh, Seong-Eun Kim, In-Hwan Jang, Seok-Min Kim, Soo Yun Lee, Sunyoung Lee, In-Sun Chu, Suk Ran Yoon, Haiyoung Jung, Inpyo Choi and 2 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature immunology, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 15 papers.

0numbers the graph read from it
0cells of the map it votes in
15citing papers in PubMed
4.3field-weighted citation impact, top 6% 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

15 citing papers in PubMed, 26 citations in OpenAlex.

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  5. Reinvigorating COTL1Nature cell biology · 2026
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

12 authors at 5 institutions in 2 countries.

Se-Chan Oh *Immunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.ORCID http://orcid.org/0000-0003-0088-7580
Seong-Eun Kim *Department of Mechanical Engineering, Pohang University of Science and Technology, Pohang, Republic of Korea.ORCID http://orcid.org/0000-0001-9367-5012
In-Hwan JangImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
Seok-Min KimImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
Soo Yun LeeImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
Sunyoung LeeImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
In-Sun ChuKorea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.ORCID http://orcid.org/0000-0001-5374-4191
Suk Ran YoonImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
Haiyoung JungImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
Inpyo ChoiImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea.
Junsang DohDepartment of Materials Science and Engineering, Research Institute of Advanced Materials, Institute of Engineering Research, Bio-MAX Institute, Soft Foundry Institute, Seoul National University, Seoul, Republic of Korea. jsdoh@snu.ac.kr.ORCID http://orcid.org/0000-0002-1483-2380
Tae-Don KimImmunotherapy Research Center, Korea Research Institute of Bioscience and Biotechnology, Daejeon, Republic of Korea. tdkim@kribb.re.kr.ORCID http://orcid.org/0000-0002-5910-4264
Korea Research Institute of Bioscience and Biotechnology · KRKorea University · KRPohang University of Science and Technology · KRInstitute for Basic Science · KRSeoul National University · KR

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

The formation of an immunological synapse (IS) is essential for natural killer (NK) cells to eliminate target cells. Despite an advanced understanding of the characteristics of the IS and its formation processes, the mechanisms that regulate its stability via the cytoskeleton are unclear. Here, we show that Nogo receptor 1 (NgR1) has an important function in modulating NK cell-mediated killing by destabilization of IS formation. NgR1 deficiency or blockade resulted in improved tumor control of NK cells by enhancing NK-to-target cell contact stability and regulating F-actin dynamics during IS formation. Patients with tumors expressing abundant NgR1 ligand had poor prognosis despite high levels of NK cell infiltration. Thus, our study identifies NgR1 as an immune checkpoint in IS formation and indicates a potential approach to improve the cytolytic function of NK cells in cancer immunotherapy.

Indexed as

Immunological SynapsesNeoplasmsActinsHumansKiller Cells, NaturalNogo Receptor 1Receptors, Natural Killer CellActinsNogo Receptor 1Receptors, Natural Killer Cell

Identifiers

PMID36624164
OpenAlexW4313893502

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.