Evidence map›Paper›PMID 34234778›Full record

ArticleFrontiers in immunology2021

High Mobility Group Box 1 (HMGB1) Induces Toll-Like Receptor 4-Mediated Production of the Immunosuppressive Protein Galectin-9 in Human Cancer Cells.

Anette Teo Hansen Selnø, Stephanie Schlichtner, Inna M Yasinska, Svetlana S Sakhnevych, Walter Fiedler, Jasmin Wellbrock, Steffen M Berger, Elena Klenova, Bernhard F Gibbs, Elizaveta Fasler-Kan and 1 more

Open access · goldAbstract read
In one paragraph

Article in Frontiers in immunology, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers.

0numbers the graph read from it
0cells of the map it votes in
19citing papers in PubMed
1.6field-weighted citation impact, top 17% 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

19 citing papers in PubMed, 27 citations in OpenAlex.

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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

11 authors at 5 institutions in 3 countries.

Anette Teo Hansen SelnøMedway School of Pharmacy, Universities of Kent and Greenwich, Chatham Maritime, United Kingdom.
Stephanie SchlichtnerMedway School of Pharmacy, Universities of Kent and Greenwich, Chatham Maritime, United Kingdom.
Inna M YasinskaMedway School of Pharmacy, Universities of Kent and Greenwich, Chatham Maritime, United Kingdom.
Svetlana S SakhnevychMedway School of Pharmacy, Universities of Kent and Greenwich, Chatham Maritime, United Kingdom.
Walter FiedlerDepartment of Oncology, Hematology and Bone Marrow Transplantation With Section Pneumology, Hubertus Wald University Cancer Center, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Jasmin WellbrockDepartment of Oncology, Hematology and Bone Marrow Transplantation With Section Pneumology, Hubertus Wald University Cancer Center, University Medical Center Hamburg-Eppendorf, Hamburg, Germany.
Steffen M BergerDepartment of Pediatric Surgery, Department of Biomedical Research, Children's Hospital, Inselspital, University of Bern, Bern, Switzerland.
Elena KlenovaSchool of Biological Sciences, University of Essex, Colchester, United Kingdom.
Bernhard F GibbsMedway School of Pharmacy, Universities of Kent and Greenwich, Chatham Maritime, United Kingdom.
Elizaveta Fasler-KanDepartment of Pediatric Surgery, Department of Biomedical Research, Children's Hospital, Inselspital, University of Bern, Bern, Switzerland.
Vadim V SumbayevMedway School of Pharmacy, Universities of Kent and Greenwich, Chatham Maritime, United Kingdom.
Medway School of Pharmacy · GBUniversity Children’s Hospital Bern · CHUniversity Cancer Center Hamburg · DEUniversity Medical Center Hamburg-Eppendorf · DEUniversity of Essex · GB

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

High mobility group box 1 (HMGB1) is a non-histone protein which is predominantly localised in the cell nucleus. However, stressed, dying, injured or dead cells can release this protein into the extracellular matrix passively. In addition, HMGB1 release was observed in cancer and immune cells where this process can be triggered by various endogenous as well as exogenous stimuli. Importantly, released HMGB1 acts as a so-called "danger signal" and could impact on the ability of cancer cells to escape host immune surveillance. However, the molecular mechanisms underlying the functional role of HMGB1 in determining the capability of human cancer cells to evade immune attack remain unclear. Here we report that the involvement of HMGB1 in anti-cancer immune evasion is determined by Toll-like receptor (TLR) 4, which recognises HMGB1 as a ligand. We found that HGMB1 induces TLR4-mediated production of transforming growth factor beta type 1 (TGF-β), displaying autocrine/paracrine activities. TGF-β induces production of the immunosuppressive protein galectin-9 in cancer cells. In TLR4-positive cancer cells, HMGB1 triggers the formation of an autocrine loop which induces galectin-9 expression. In malignant cells lacking TLR4, the same effect could be triggered by HMGB1 indirectly through TLR4-expressing myeloid cells present in the tumour microenvironment (e. g. tumour-associated macrophages).

Indexed as

GalectinsHMGB1 ProteinHumansImmune ToleranceNeoplasmsTHP-1 CellsToll-Like Receptor 4Transforming Growth Factor beta1GalectinsHMGB1 ProteinLGALS9 protein, humanTGFB1 protein, humanTLR4 protein, humanToll-Like Receptor 4Transforming Growth Factor beta1galectin-9HMGB1 (high mobility group box 1)immune surveillanceTGF-beta 1Toll-like receptors

Identifiers

PMID34234778
PMCPMC8255966
OpenAlexW3173614841

What OpenQuestion holds

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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.