Evidence map›Paper›PMID 41963299›Full record

ArticleCell death & disease2026

Plasmodium yoelii infection induces lung injury by modulating type 2 conventional dendritic cells autophagy via the STAT3-IRF4 signaling.

Cansheng Hong, Guorong Deng, Zhihan Jiang, Yishuai Lu, Qianlian Wu, Chao Huang, Jia Tang, Haiqi Zhou, Qinan Liu, Xiujuan Luo and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Cell death & disease, 2026. 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

15 authors.

Cansheng Hong *Department of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Guorong Deng *Department of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Zhihan Jiang *Department of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Yishuai LuDepartment of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Qianlian WuDepartment of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Chao HuangDepartment of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Jia TangState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China.
Haiqi ZhouDepartment of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Qinan LiuDepartment of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Xiujuan LuoDepartment of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Yi ZhaoDepartment of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Yanwei QiDepartment of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Qingqing LiDepartment of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China.
Xiancai MaState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, the First Affiliated Hospital of Guangzhou Medical University, Guangzhou, China. ma_xiancai@gzlab.ac.cn.ORCID http://orcid.org/0000-0002-4934-4221
Quan YangDepartment of Pathogenic Biology and Immunology, Sino-French Hoffmann Institute, School of Basic Medical Sciences, Guangzhou Medical University, Guangzhou, China. yquangy2015@gzhmu.edu.cn.ORCID http://orcid.org/0000-0002-2778-6862

Funding

National Natural Science Foundation of China (National Science Foundation of China) 82471791
6 · The paper itself

Abstract

Malaria is an infectious disease caused by Plasmodium that severely impacts human health, often resulting in lung injury. Classical type 2 dendritic cells (cDC2) in the lungs play a crucial role in the pathogenesis of asthma and infectious diseases; however, their specific functions during Plasmodium infection remain poorly understood. In this study, we demonstrated a significant accumulation and activation of cDC2 in the lungs of mice infected with Plasmodium. While the phagocytosis ability of activated cDC2 decreases, it promotes the differentiation of CD4

Indexed as

AutophagyDendritic CellsInterferon Regulatory FactorsLung InjuryMalariaPlasmodium yoeliiSTAT3 Transcription FactorAnimalsLungMiceMice, Inbred C57BLPhagocytosisSignal TransductionTh1 CellsInterferon Regulatory FactorsStat3 protein, mouseSTAT3 Transcription Factor

Identifiers

PMID41963299
PMCPMC13181017

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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.