Evidence map›Paper›PMID 41761269›Full record

ArticleParasites & vectors2026

TGF-β regulated Tim-3 sustains macrophage phagocytic function and confers protection in Plasmodium yoelii NSM-infected mice.

Xiongyu Xie, Guikuan Liang, Mingjie Chen, Lixin Luo, Haiwen Yuan, Shenao Chen, Keyu Lu, Wenbo Peng, Long Xu, Hongyan Xie and 5 more

Abstract read
In one paragraph

Article in Parasites & vectors, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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0citing papers in PubMed
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1 · What the graph read from it

What it found

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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

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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

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0 citing papers in PubMed.

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4 · The record

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5 · Who and what money

Authors and funding

15 authors.

Xiongyu Xie *Department of Infectious Diseases, Key Laboratory for Major Obstetric Diseases of Guangdong Province, The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Guikuan Liang *Department of Infectious Diseases, Key Laboratory for Major Obstetric Diseases of Guangdong Province, The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Mingjie Chen *Key Laboratory of Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Lixin LuoKey Laboratory of Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Haiwen YuanDepartment of Infectious Diseases, Key Laboratory for Major Obstetric Diseases of Guangdong Province, The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, China.
Shenao ChenKey Laboratory of Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Keyu LuKey Laboratory of Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Wenbo PengKey Laboratory of Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Long XuKey Laboratory of Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Hongyan XieKey Laboratory of Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Lu LiKey Laboratory of Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Shan ZhaoKey Laboratory of Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Haixia WeiKey Laboratory of Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China. weihaixia2012@sina.com.
Xingfei PanDepartment of Infectious Diseases, Key Laboratory for Major Obstetric Diseases of Guangdong Province, The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, China. panxf0125@163.com.
Jun HuangDepartment of Infectious Diseases, Key Laboratory for Major Obstetric Diseases of Guangdong Province, The Third Affiliated Hospital, Guangzhou Medical University, Guangzhou, China. hj165@sina.com.

Funding

Bureau of Education of Guangzhou Municipality 2024312113Guangdong Medical Research Foundation B2023344Guangzhou Municipal Science and Technology Project 2025A04J3880National Natural Science Foundation of China 82271798National Outstanding Youth Science Fund Project of National Natural Science Foundation of China 82301998Natural Science Foundation of Guangdong Province 2024A1515010849Natural Science Foundation of Guangdong Province 2025A1515010418
6 · The paper itself

Abstract

backgroundT-cell immunoglobulin and mucin domain 3 (Tim-3) is a critical immune checkpoint, yet its role in regulating macrophage function during malaria infection remains poorly understood.

methodsWe established a Plasmodium yoelii NSM murine model, in vitro co-culture systems, and comprehensive techniques including scRNA-seq, flow cytometry, and functional assays to investigate Tim-3 expression on splenic macrophages and its immunoregulatory impact.

resultsWe observed a significant infection-induced downregulation of Tim-3 on splenic macrophages. Transcriptomic profiling revealed that Tim-3

conclusionsOur results reveal a novel protective TGF-β-Tim-3 axis that maintains the phagocytic function of macrophages and immune homeostasis in Plasmodium yoelii NSM infection. These findings highlight Tim-3 on macrophages as a potential therapeutic target for modulating host defense against malaria infection.

Indexed as

Hepatitis A Virus Cellular Receptor 2MacrophagesMalariaPhagocytosisPlasmodium yoeliiTransforming Growth Factor betaAnimalsDisease Models, AnimalFemaleMiceReactive Oxygen SpeciesHavcr2 protein, mouseHepatitis A Virus Cellular Receptor 2Reactive Oxygen SpeciesTransforming Growth Factor betaMacrophageMalariaPhagocytosisTGF-βTim-3

Identifiers

PMID41761269
PMCPMC13040716

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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.