Evidence map›Paper›PMID 41212476›Full record

ArticleMolecular biomedicine2025

STAT3 regulates NK and NKT cell differentiation through C-X3-C motif chemokine receptor 1  (CX3CR1) in hyper-IgE syndrome.

Ju Liu, Jingzhi Yang, Jianing Tang, Hongxia Tang, Xin Dai, Peiyao Jin, Yanmei Huang, Zhenzhen Li, Ziyin Zhang, Xiaohuan Guo and 3 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Molecular biomedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

0numbers the graph read from it
0cells of the map it votes in
0citing 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

0 citing papers in PubMed.

No citing paper in PubMed yet.

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

13 authors.

Ju LiuDepartment of Pathogen Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
Jingzhi YangDepartment of Orthopedics, Qilu Hospital of Shandong University, Jinan, Shandong, China.
Jianing TangDepartment of Pathogen Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
Hongxia TangWuhan Children's Hospital, Tongji Medical College, Huazhong University of Science & Technology, Wuhan, China.
Xin DaiCentral People's Hospital of Zhanjiang, Zhanjiang, China.
Peiyao JinDepartment of Immunology, School of Medicine, Yangtze University, Jingzhou, China.
Yanmei HuangDepartment of Pathogen Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
Zhenzhen LiDepartment of Pathogen Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
Ziyin ZhangDepartment of Pathogen Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China.
Xiaohuan GuoInstitute for Immunology, Tsinghua University, Beijing, China.
Martin BitzanKidney Centre of Excellence, Al Jalila Children's Hospital, Dubai, United Arab Emirates.
Xiaoling YinDepartment of Pediatrics, Tongji Medical College of Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China. yinxiaoling2021@tjh.tjmu.edu.cn.
Chaohong LiuDepartment of Pathogen Biology, School of Basic Medicine, Tongji Medical College and State Key Laboratory for Diagnosis and Treatment of Severe Zoonotic Infectious Diseases, Huazhong University of Science and Technology, Wuhan, 430030, Hubei, China. chaohongliu80@126.com.ORCID 0000-0001-7028-4625

Funding

International scientific and technological innovation cooperation between governments from Ministry of Science and Technology of the People's Republic of China 2021YFE0108200National Key R&D Program of China 2023YFC2507900National Key R&D Program of China 2023YFC2706300National Natural Science Foundation of China 32100709National Natural Science Foundation of China 82371784National Natural Science Foundation of China NSFC32311530061
6 · The paper itself

Abstract

Mutations in the signal transducer and activator of transcription 3 (STAT3) gene are strongly associated with Hyper-IgE Syndrome (HIES), a rare immunodeficiency disorder characterized by elevated levels of IgE and recurrent infections. The molecular mechanisms of how STAT3 dysfunction contributes to the pathophysiology of HIES are complex and not fully elucidated, especially in natural killer (NK) cells, which are crucial for the immune response against infections and malignancies. Employing single-cell sequencing and flow cytometry, we investigated the effects of STAT3 mutations on immune cell development, differentiation, and function. Our findings revealed an increased population of CX3CR1

Indexed as

Cell DifferentiationCX3C Chemokine Receptor 1Job SyndromeKiller Cells, NaturalNatural Killer T-CellsSTAT3 Transcription FactorAnimalsFemaleHumansImmunoglobulin EInterleukin-4MaleMiceMice, KnockoutMutationCX3C Chemokine Receptor 1Immunoglobulin EInterleukin-4STAT3 protein, humanSTAT3 Transcription FactorC-X3-C motif chemokine receptor 1Hyper-IgE syndromeNK cellsSTAT3 mutation

Identifiers

PMID41212476
PMCPMC12602802

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.