Evidence map›Paper›PMID 34381181›Full record

ArticleLeukemia2022

Regulatory T cells promote the stemness of leukemia stem cells through IL10 cytokine-related signaling pathway.

Yingxi Xu, Junli Mou, Ying Wang, Wei Zhou, Qing Rao, Haiyan Xing, Zheng Tian, Kejing Tang, Min Wang, Jianxiang Wang

Erratum issuedAbstract read
PubMed Publisher
In one paragraph

Article in Leukemia, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 42 papers.

0numbers the graph read from it
0cells of the map it votes in
42citing papers in PubMed
3.4field-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

42 citing papers in PubMed, 62 citations in OpenAlex.

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  14. CD4Science advances · 2025
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  15. Review
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  19. Review
  20. Prognostic analysis of SYTL4 in acute myeloid leukemia.Translational cancer research · 2024
    Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

10 authors at 2 institutions in 1 country.

Yingxi XuState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China.ORCID http://orcid.org/0000-0002-0056-7440
Junli MouState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China.
Ying WangState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China.
Wei ZhouSchool of Medicine, Nankai University, Tianjin, China.
Qing RaoState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China.ORCID http://orcid.org/0000-0001-6721-1337
Haiyan XingState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China.
Zheng TianState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China.
Kejing TangState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China.
Min WangState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China. wangjxm@ihcams.ac.cn.ORCID http://orcid.org/0000-0003-1637-0324
Jianxiang WangState Key Laboratory of Experimental Hematology, Institute of Hematology and Blood Diseases Hospital, Chinese Academy of Medical Sciences & Peking Union Medical College, Tianjin, China. wangjx@ihcams.ac.cn.ORCID http://orcid.org/0000-0001-9437-9151
Chinese Academy of Medical Sciences & Peking Union Medical College · CNNankai University · CN

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Regulatory T cells (Tregs) could maintain the characteristics of stem cells and inhibit the differentiation of normal hematopoietic stem/progenitor cells. Recent studies have shown that Tregs, as an important component of acute myeloid leukemia (AML) microenvironments, can help AML cells to evade immune surveillance. However, their function in directly regulating the stemness of AML cells remains elusive. In this study, the increased stemness of AML cells promoted by Tregs was verified in vitro and in vivo. The cytokines released by Tregs were explored, the highly expressed anti-inflammatory cytokine IL10 was found, which could promote the stemness of AML cells through the activation of PI3K/AKT signal pathway. Moreover, disrupting the IL10/IL10R/PI3K/AKT signal in AML/ETO c-kit

Indexed as

Cell DifferentiationCell ProliferationHumansInterleukin-10Leukemia, Myeloid, AcuteNeoplastic Stem CellsPhosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Interleukin-10Signal TransductionT-Lymphocytes, RegulatoryTumor Cells, CulturedTumor MicroenvironmentIL10 protein, humanInterleukin-10Phosphatidylinositol 3-KinasesProto-Oncogene Proteins c-aktReceptors, Interleukin-10

Identifiers

PMID34381181
OpenAlexW3187124736

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.