Evidence map›Paper›PMID 39609883›Full record

ArticleParasites & vectors2024

IRF4 regulates myeloid-derived suppressor cells expansion and function in Schistosoma japonicum-infected mice.

Lu Zhou, Peibin Lin, Guorong Deng, Lengshan Mo, Cansheng Hong, Zhihan Jiang, Yiqiang Zhu, Yi Zhao, Yanwei Qi, Tengfei Hu and 4 more

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PubMed Full text at PMC Publisher
In one paragraph

Article in Parasites & vectors, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing papers in PubMed
–field-weighted citation impact
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

2 citing papers in PubMed.

  1. Review
  2. T cell exhaustion in parasitic infections.Frontiers in immunology · 2026
    Review
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

14 authors.

Lu Zhou *Affiliated Qingyuan Hospital, Qingyuan People's Hospital, Guangzhou Medical University, Qingyuan, 511518, China.
Peibin Lin *Affiliated Qingyuan Hospital, Qingyuan People's Hospital, Guangzhou Medical University, Qingyuan, 511518, China.
Guorong Deng *Department of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 511436, China.
Lengshan MoDepartment of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 511436, China.
Cansheng HongDepartment of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 511436, China.
Zhihan JiangDepartment of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 511436, China.
Yiqiang ZhuDepartment of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 511436, China.
Yi ZhaoDepartment of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 511436, China.
Yanwei QiDepartment of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 511436, China.
Tengfei HuDepartment of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 511436, China.
Qianlian WuDepartment of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 511436, China.
Jian ZhangSchool of Biomedical Engineering, Guangzhou Medical University, Guangzhou, 511436, China. jianzhang@gzhmu.edu.cn.
Qingqing LiDepartment of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, 511436, China. 179709984@qq.com.
Quan YangAffiliated Qingyuan Hospital, Qingyuan People's Hospital, Guangzhou Medical University, Qingyuan, 511518, China. yquangy2015@gzhmu.edu.cn.

Funding

Medical Scientific Research Foundation of Guangdong Province A2024163National Key R&D Program of China 2022YFC2304205National Natural Science Foundation of China 82471791Project supported by the Discipline Construction Fund of Guangzhou Medical University JCXKJS2021C08Students' Innovation Ability Enhancement Plan project of Guangzhou Medical University PX-66221466Tertiary Education Scientific research project of Guangzhou Municipal Education Bureau 2024312082The open research funds from the Sixth Affiliated Hospital of Guangzhou Medical University, Qingyuan People's Hospital 202301-404
6 · The paper itself

Abstract

backgroundInterferon regulatory factor 4 (IRF4) is a crucial member of the IRF family of transcription factors and is pivotal in orchestrating the body's defense against tumors and infections by modulating the differentiation and functionality of immune cells. The role of IRF4 in mice during Schistosoma japonicum infection, as well as the effects of IRF4 deficiency on myeloid-derived suppressor cells (MDSCs), remains inadequately understood.

methodsHematoxylin and eosin staining was used to evaluate the pathological damage in different organs of mice following infection with S. japonicum. Flow cytometry was employed to study the effect of IRF4 on the proliferation and function of myeloid-derived suppressor cells (MDSCs) in S. japonicum-infected mice.

resultsKnockout of IRF4 in myeloid cells significantly mitigated pathological damage to the liver and lungs in mice infected with S. japonicum. Knockout of IRF4 in myeloid cells also inhibited the expansion and functionality of MDSCs by downregulating programmed death ligand 2 (PD-L2) expression and interleukin-1 alpha (IL-1α) secretion in mice infected with S. japonicum. Mechanistic studies revealed that IRF4 deficiency inhibited the expansion and function of MDSCs and that this inhibition was mediated by the STAT3 and AKT signaling pathways. Also, IRF4 myeloid knockout promoted the expansion of T cells in S. japonicum-infected mice, but had no significant effect on B cell aggregation.

conclusionsOverall, these findings highlight the importance of IRF4 in regulating MDSCs and their impact on tissue damage during S. japonicum infection, providing valuable insights into potential therapeutic targets for managing the pathological consequences of this parasitic infection.

Indexed as

Interferon Regulatory FactorsMyeloid-Derived Suppressor CellsSchistosoma japonicumSchistosomiasis japonicaAnimalsCell ProliferationFemaleInterferon Regulatory Factor-4LiverMiceMice, Inbred C57BLMice, KnockoutSignal TransductionInterferon Regulatory Factor-4Interferon Regulatory FactorsInfectionInterferon regulatory factor 4Myeloid-derived suppressor cellSchistosoma japonicum

Identifiers

PMID39609883
PMCPMC11605884

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