Evidence map›Paper›PMID 31662347›Full record

ArticleThe Journal of experimental medicine2020

TIPE2 specifies the functional polarization of myeloid-derived suppressor cells during tumorigenesis.

Dehong Yan, Jinghui Wang, Honghong Sun, Ali Zamani, Honglin Zhang, Weihong Chen, Aifa Tang, Qingguo Ruan, Xiaolu Yang, Youhai H Chen and 1 more

Open access · bronzeAbstract read
In one paragraph

Article in The Journal of experimental medicine, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 47 papers, 1 of them a synthesis that pooled it.

0numbers the graph read from it
0cells of the map it votes in
47citing papers in PubMed, 1 pooled it
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

47 citing papers in PubMed, 1 synthesis or guideline pooled it, 69 citations in OpenAlex.

  1. Pooled it
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  16. MDSC: a new potential breakthrough in CAR-T therapy for solid tumors.Cell communication and signaling : CCS · 2024
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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 2 countries.

Dehong YanShenzhen Laboratory for Human Antibody Engineering, Center for Protein and Cell-based Drugs, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China.
Jinghui WangShenzhen Laboratory for Human Antibody Engineering, Center for Protein and Cell-based Drugs, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China.
Honghong SunDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
Ali ZamaniDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
Honglin ZhangShenzhen Laboratory for Human Antibody Engineering, Center for Protein and Cell-based Drugs, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China.
Weihong ChenDepartment of Hematology, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People's Hospital, Shenzhen, China.
Aifa TangDepartment of Hematology, The First Affiliated Hospital of Shenzhen University, Shenzhen Second People's Hospital, Shenzhen, China.
Qingguo RuanShenzhen Laboratory for Human Antibody Engineering, Center for Protein and Cell-based Drugs, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China.
Xiaolu YangAbramson Family Cancer Research Institute, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
Youhai H ChenDepartment of Pathology and Laboratory Medicine, Perelman School of Medicine, University of Pennsylvania, Philadelphia, PA.
Xiaochun WanShenzhen Laboratory for Human Antibody Engineering, Center for Protein and Cell-based Drugs, Shenzhen Institutes of Advanced Technology, Chinese Academy of Sciences, Shenzhen, China.
Chinese Academy of Sciences · CNUniversity of Pennsylvania · USShenzhen Second People's Hospital · CNCancer Research Institute · USJinan University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Myeloid-derived suppressor cells (MDSCs) are "polarized" myeloid cells that effectively promote tumorigenesis by inhibiting antitumor immunity. How myeloid cells acquire the protumoral properties during tumorigenesis is poorly understood. We report here that the polarity protein TIPE2 (tumor necrosis factor-α-induced protein 8-like 2) mediates the functional polarization of murine and human MDSCs by specifying their pro- and antitumoral properties. Tumor cells induced the expression of TIPE2 in Gr1+CD11b+ cells through reactive oxygen species (ROS). TIPE2 in turn increased the expression of protumoral mediators such as CCAAT/enhancer-binding protein-β while inhibiting the expression of antitumoral mediators. Consequently, tumor growth in TIPE2-deficient mice was significantly diminished, and TIPE2-deficient MDSCs markedly inhibited tumor growth upon adoptive transfer. Pharmaceutical blockade of ROS inhibited TIPE2 expression in MDSCs and reduced tumor growth in mice. These findings indicate that TIPE2 plays a key role in the functional polarization of MDSCs and represents a new therapeutic target for cancer immunotherapy.

Indexed as

AcetylcysteineAdoptive TransferAnimalsCarcinogenesisCell PolarityCell Transformation, NeoplasticFemaleHEK293 CellsHumansIntracellular Signaling Peptides and ProteinsLung NeoplasmsLysineMaleMiceMice, Inbred C57BLMice, KnockoutAcetylcysteineIntracellular Signaling Peptides and ProteinsLysineN-acetylcysteine lysinateReactive Oxygen SpeciesTIPE2 protein, mouseTNFAIP8L2 protein, human

Identifiers

PMID31662347
PMCPMC7041705
OpenAlexW2982350192

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-SA
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.