Evidence map›Paper›PMID 34686865›Full record

ArticleNature immunology2021

Epithelial cells remove precancerous cells by cell competition via MHC class I-LILRB3 interaction.

Shiyu Ayukawa, Nagisa Kamoshita, Jun Nakayama, Ryohei Teramoto, Novalia Pishesha, Kenji Ohba, Nanami Sato, Kei Kozawa, Hikari Abe, Kentaro Semba and 3 more

Abstract read
PubMed Publisher
In one paragraph

Article in Nature immunology, 2021. 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
2.4field-weighted citation impact, top 10% 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, 43 citations in OpenAlex.

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  14. An expanded view of cell competition.Development (Cambridge, England) · 2024
    Review
  15. Article
  16. Article
  17. A Hierarchical Mechanotransduction System: From Macro to Micro.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2024
    Review
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4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

13 authors at 4 institutions in 2 countries.

Shiyu AyukawaDepartment of Life Science and Medical Bioscience, School of Advanced Science and Engineering, Waseda University, Tokyo, Japan.
Nagisa Kamoshita *Waseda Institute for Advanced Study, Waseda University, Tokyo, Japan.
Jun Nakayama *Department of Life Science and Medical Bioscience, School of Advanced Science and Engineering, Waseda University, Tokyo, Japan.ORCID http://orcid.org/0000-0001-8844-4295
Ryohei TeramotoDepartment of Life Science and Medical Bioscience, School of Advanced Science and Engineering, Waseda University, Tokyo, Japan.
Novalia PisheshaFaculty of Arts and Sciences, Harvard University, Cambridge, MA, USA.
Kenji OhbaDivision of Genetic Therapeutics, Center for Molecular Medicine, Jichi Medical University, Tochigi, Japan.ORCID http://orcid.org/0000-0002-4936-8186
Nanami SatoDivision of Molecular Oncology, Institute for Genetic Medicine, Hokkaido University Graduate School of Chemical Sciences and Engineering, Hokkaido, Japan.
Kei KozawaDivision of Molecular Oncology, Institute for Genetic Medicine, Hokkaido University Graduate School of Chemical Sciences and Engineering, Hokkaido, Japan.
Hikari AbeDepartment of Life Science and Medical Bioscience, School of Advanced Science and Engineering, Waseda University, Tokyo, Japan.
Kentaro SembaDepartment of Life Science and Medical Bioscience, School of Advanced Science and Engineering, Waseda University, Tokyo, Japan.
Nobuhito GodaDepartment of Life Science and Medical Bioscience, School of Advanced Science and Engineering, Waseda University, Tokyo, Japan.
Yasuyuki FujitaDivision of Molecular Oncology, Institute for Genetic Medicine, Hokkaido University Graduate School of Chemical Sciences and Engineering, Hokkaido, Japan.
Takeshi MaruyamaWaseda Institute for Advanced Study, Waseda University, Tokyo, Japan. tmaru@aoni.waseda.jp.ORCID http://orcid.org/0000-0003-0331-4702
Waseda University · JPHokkaido University · JPHarvard University · USJichi Medical University · JP

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Epithelial cells have an ability termed 'cell competition', which is an immune surveillance-like function that extrudes precancerous cells from the epithelial layer, leading to apoptosis and clearance. However, it remains unclear how epithelial cells recognize and extrude transformed cells. Here, we discovered that a PirB family protein, leukocyte immunoglobulin-like receptor B3 (LILRB3), which is expressed on non-transformed epithelial cells, recognizes major histocompatibility complex class I (MHC class I) that is highly expressed on transformed cells. MHC class I interaction with LILRB3 expressed on normal epithelial cells triggers an SHP2-ROCK2 pathway that generates a mechanical force to extrude transformed cells. Removal of transformed cells occurs independently of natural killer (NK) cell or CD8

Indexed as

ApoptosisCell CompetitionAnimalsAntigens, CDCore Binding Factor Alpha 1 SubunitDogsEpithelial CellsHaCaT CellsHistocompatibility Antigens Class IHumansLung NeoplasmsMadin Darby Canine Kidney CellsMechanotransduction, CellularMiceMice, Inbred BALB CMice, NudeAntigens, CDCore Binding Factor Alpha 1 SubunitHistocompatibility Antigens Class ILILRB3 protein, humanProtein Tyrosine Phosphatase, Non-Receptor Type 11PTPN11 protein, humanReceptors, Immunologicrho-Associated KinasesROCK2 protein, humanRUNX2 protein, human

Identifiers

PMID34686865
OpenAlexW3206700678

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.