Evidence map›Paper›PMID 39181199›Full record

ArticleJournal of advanced research2025

Dual nature of type I interferon responses and feedback regulations by SOCS1 dictate malaria mortality.

Jiansen Lu, Zhiqiang Hu, Huaji Jiang, Zebin Wen, Hongyu Li, Jian Li, Ke Zeng, Yingchao Xie, Huadan Chen, Xin-Zhuan Su and 2 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Journal of advanced research, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 3 papers.

0numbers the graph read from it
0cells of the map it votes in
3citing 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

3 citing papers in PubMed.

  1. Article
  2. Article
  3. Type I Interferon Signaling Augments Autoimmunity in Neuromyelitis Optica Spectrum Disorder.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2025
    Article
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

12 authors.

Jiansen LuDepartment of Joint Surgery, the Fifth Affiliated Hospital of Southern Medical University, Department of Immunology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, China.
Zhiqiang HuDepartment of Joint Surgery, the Fifth Affiliated Hospital of Southern Medical University, Department of Immunology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, China; Zhejiang Provincial Key Laboratory of Pancreatic Disease, The First Affiliated Hospital, Institute of Translational Medicine, Zhejiang University School of Medicine, Zhejiang University, Hangzhou, Zhejiang 310029, China.
Huaji JiangDepartment of Joint Surgery, the Fifth Affiliated Hospital of Southern Medical University, Department of Immunology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, China.
Zebin WenGuangdong Provincial Key Lab of Single Cell Technology and Application, Southern Medical University, Guangzhou, Guangdong 510515, China.
Hongyu LiDepartment of Joint Surgery, the Fifth Affiliated Hospital of Southern Medical University, Department of Immunology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, China.
Jian LiState Key Laboratory of Cellular Stress Biology, Innovation Center for Cell Biology, School of Life Sciences, Xiamen University, Xiamen, Fujian 361000, China.
Ke ZengDepartment of Joint Surgery, the Fifth Affiliated Hospital of Southern Medical University, Department of Immunology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, China.
Yingchao XieDepartment of Joint Surgery, the Fifth Affiliated Hospital of Southern Medical University, Department of Immunology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, China.
Huadan ChenDepartment of Joint Surgery, the Fifth Affiliated Hospital of Southern Medical University, Department of Immunology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, China.
Xin-Zhuan SuMalaria Functional Genomics Section, Laboratory of Malaria and Vector Research, National Institute of Allergy and Infectious Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
Chunmei CaiResearch Center for High Altitude Medicine, School of Medical, Key Laboratory of Application and Foundation for High Altitude Medicine Research in Qinghai Province, Qinghai University, Xining, Qinghai 810000, China. Electronic address: caicm@qhu.edu.cn.
Xiao YuDepartment of Joint Surgery, the Fifth Affiliated Hospital of Southern Medical University, Department of Immunology, School of Basic Medical Sciences, Southern Medical University, Guangzhou, Guangdong 510515, China; Guangdong Provincial Key Lab of Single Cell Technology and Application, Southern Medical University, Guangzhou, Guangdong 510515, China; Department of Clinical Laboratory Medicine, Guangdong Provincial People's Hospital (Guangdong Academy of Medical Sciences), Southern Medical University, Guangzhou, Guangdong 510000, China. Electronic address: xiaoyu523@smu.edu.cn.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

introductionType I interferon (IFN-I, IFN-α/β), precisely controlled by multiple regulators, including suppressor of cytokine signaling 1 (SOCS1), is critical for host defense against pathogens. However, the impact of IFN-α/β on malaria parasite infections, beneficial or detrimental, remains controversial.

objectivesThe contradictory results are suspected to arise from differences in parasite species and host genetic backgrounds. To date, no prior study has employed a comparative approach utilizing two parasite models to investigate the underlying mechanisms of IFN-I response. Moreover, whether and how SOCS1 involves in the distinct IFN-α/β dynamics is still unclear.

methodsHere we perform single-cell RNA sequencing analyses (scRNA-seq) to dissect the dynamics of IFN-α/β responses against P. yoelii 17XL (17XL) and P. berghei ANKA (PbANKA) infections; conduct flow cytometry analysis and functional depletion to identify key cellular players induced by IFN-I; and establish mathematical models to explore the mechanisms underlying the differential IFN-I dynamics regulated by SOCS1.

results17XL stimulates an early protective but insufficient toll-like receptor 7 (TLR7)-interferon regulatory factor 7 (IRF7)-dependent IFN-α/β response, resulting in CD11a

conclusionThis study reveals the dual functions of IFN-I in anti-malarial immunity: Early IFN-α/β enhances immune responses against Plasmodium infection by promoting CD11a

Indexed as

Interferon Type IMalariaSuppressor of Cytokine Signaling 1 ProteinAnimalsFeedback, PhysiologicalInterferon-betaInterferon Regulatory Factor-7MiceMice, Inbred C57BLPlasmodium yoeliiSingle-Cell AnalysisInterferon-betaInterferon Regulatory Factor-7Interferon Type ISocs1 protein, mouseSuppressor of Cytokine Signaling 1 ProteinFeedback regulationMathematical modelingPlasmodiumscRNA-seqSOCS1Type I IFN

Identifiers

PMID39181199
PMCPMC12225910

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Registered trials

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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.