Evidence map›Paper›PMID 37432112›Full record

ArticleCancer immunology research2023

Clec4A4 Acts as a Negative Immune Checkpoint Regulator to Suppress Antitumor Immunity.

Tomofumi Uto, Tomohiro Fukaya, Shuya Mitoma, Yotaro Nishikawa, Moe Tominaga, Narantsog Choijookhuu, Yoshitaka Hishikawa, Katsuaki Sato

Open access · hybridAbstract read
In one paragraph

Article in Cancer immunology research, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing papers in PubMed
1.3field-weighted citation impact, top 19% 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

6 citing papers in PubMed, 8 citations in OpenAlex.

  1. Article
  2. Review
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  4. A potential XGBoost Diagnostic Score forFrontiers in immunology · 2025
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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

8 authors at 1 institution in 1 country.

Tomofumi UtoDivision of Immunology, Department of Infectious Diseases, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.ORCID 0009-0002-5298-4681
Tomohiro FukayaDivision of Immunology, Department of Infectious Diseases, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.ORCID 0000-0003-1633-3232
Shuya MitomaDivision of Immunology, Department of Infectious Diseases, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.ORCID 0000-0003-4271-0150
Yotaro NishikawaDivision of Immunology, Department of Infectious Diseases, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.ORCID 0000-0002-4796-9711
Moe TominagaDivision of Immunology, Department of Infectious Diseases, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.ORCID 0009-0001-1333-8399
Narantsog ChoijookhuuDivision of Histochemistry and Cell Biology, Department of Anatomy, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.ORCID 0000-0002-3398-4785
Yoshitaka HishikawaDivision of Histochemistry and Cell Biology, Department of Anatomy, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.ORCID 0000-0002-3796-6234
Katsuaki SatoDivision of Immunology, Department of Infectious Diseases, Faculty of Medicine, University of Miyazaki, Miyazaki, Japan.ORCID 0000-0002-1844-6620
University of Miyazaki · JP

Funding

Japan Agency for Medical Research and Development (AMED) 22ama221311h0001Ministry of Education, Science and Culture of Japan 20K07703Ministry of Education, Science and Culture of Japan 22H02924
6 · The paper itself

Abstract

Clec4A4 is a C-type lectin receptor (CLR) exclusively expressed on murine conventional dendritic cells (cDC) to regulate their activation status. However, the functional role of murine Clec4A4 (mClec4A4) in antitumor immunity remains unclear. Here, we show that mClec4A4 serves as a negative immune checkpoint regulator to impair antitumor immune responses. Deficiency of mClec4A4 lead to a reduction in tumor development, accompanied by enhanced antitumor immune responses and amelioration of the immunosuppressive tumor microenvironment (TME) mediated through the enforced activation of cDCs in tumor-bearing mice. Furthermore, antagonistic mAb to human CLEC4A (hCLEC4A), which is the functional orthologue of mClec4A4, exerted protection against established tumors without any apparent signs of immune-related adverse events in hCLEC4A-transgenic mice. Thus, our findings highlight the critical role of mClec4A4 expressed on cDCs as a negative immune checkpoint molecule in the control of tumor progression and provide support for hCLEC4A as a potential target for immune checkpoint blockade in tumor immunotherapy.

Indexed as

Lectins, C-TypeNeoplasmsAnimalsCell Line, TumorDendritic CellsHumansImmunotherapyMiceMice, Inbred C57BLMice, KnockoutMice, TransgenicTumor MicroenvironmentLectins, C-Type

Identifiers

PMID37432112
PMCPMC10472101
OpenAlexW4383873063

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.