Evidence map›Paper›PMID 42364976›Full record

ArticleNature communications2026

Splenic macrophage-B cell axis drives systemic autoimmune-like pathology in Cerebral Malaria.

Xin Sun, Ridong Li, Weixuan Wang, Danli Yang, Wenyu Tian, Xin Zhang, Linjiang Han, Xuyang Zhao, Xiaoyan Xing, Runtao Li and 5 more

Abstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Nature communications, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing 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

1 citing paper in PubMed.

  1. 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

15 authors.

Xin Sun *Institute of Systems Biomedicine, Department of Microbiology and Infectious Disease Center, School of Basic Medical Sciences, Beijing Key Laboratory of Advanced Pharmaceutical Preparation, Peking University, Beijing, China.
Ridong Li *Institute of Systems Biomedicine, Department of Microbiology and Infectious Disease Center, School of Basic Medical Sciences, Beijing Key Laboratory of Advanced Pharmaceutical Preparation, Peking University, Beijing, China.ORCID http://orcid.org/0000-0001-6988-8894
Weixuan Wang *Institute of Systems Biomedicine, Department of Microbiology and Infectious Disease Center, School of Basic Medical Sciences, Beijing Key Laboratory of Advanced Pharmaceutical Preparation, Peking University, Beijing, China.
Danli Yang *Institute of Systems Biomedicine, Department of Microbiology and Infectious Disease Center, School of Basic Medical Sciences, Beijing Key Laboratory of Advanced Pharmaceutical Preparation, Peking University, Beijing, China.
Wenyu TianInstitute of Systems Biomedicine, Department of Microbiology and Infectious Disease Center, School of Basic Medical Sciences, Beijing Key Laboratory of Advanced Pharmaceutical Preparation, Peking University, Beijing, China.
Xin ZhangInstitute of Systems Biomedicine, Department of Microbiology and Infectious Disease Center, School of Basic Medical Sciences, Beijing Key Laboratory of Advanced Pharmaceutical Preparation, Peking University, Beijing, China.
Linjiang HanInstitute of Systems Biomedicine, Department of Microbiology and Infectious Disease Center, School of Basic Medical Sciences, Beijing Key Laboratory of Advanced Pharmaceutical Preparation, Peking University, Beijing, China.
Xuyang ZhaoInstitute of Systems Biomedicine, Department of Microbiology and Infectious Disease Center, School of Basic Medical Sciences, Beijing Key Laboratory of Advanced Pharmaceutical Preparation, Peking University, Beijing, China.ORCID http://orcid.org/0000-0002-4470-7986
Xiaoyan XingDepartment of Rheumatology and Immunology and Beijing Key Laboratory for Rheumatism and Immune Diagnosis (BZ0135), Peking University People's Hospital, Beijing, China.
Runtao LiState Key Laboratory of Natural and Biomimetic Drugs, School of Pharmaceutical Sciences, Peking University, Beijing, China.
Yuhui LiDepartment of Rheumatology and Immunology and Beijing Key Laboratory for Rheumatism and Immune Diagnosis (BZ0135), Peking University People's Hospital, Beijing, China.
Jing HeDepartment of Rheumatology and Immunology and Beijing Key Laboratory for Rheumatism and Immune Diagnosis (BZ0135), Peking University People's Hospital, Beijing, China.ORCID http://orcid.org/0000-0003-3904-8928
Rui SongNational Key Laboratory of Intelligent Tracking and Forecasting for Infectious Diseases, Beijing Institute of Infectious Diseases, Beijing Ditan Hospital, Capital Medical University, Beijing, China. songruii@hotmail.com.
Fuping YouInstitute of Systems Biomedicine, Department of Microbiology and Infectious Disease Center, School of Basic Medical Sciences, Beijing Key Laboratory of Advanced Pharmaceutical Preparation, Peking University, Beijing, China. fupingyou@pku.edu.cn.
Dan LuInstitute of Systems Biomedicine, Department of Microbiology and Infectious Disease Center, School of Basic Medical Sciences, Beijing Key Laboratory of Advanced Pharmaceutical Preparation, Peking University, Beijing, China. taotao@bjmu.edu.cn.ORCID http://orcid.org/0000-0002-3000-5094

Funding

National Natural Science Foundation of China (National Science Foundation of China) 32571053National Natural Science Foundation of China (National Science Foundation of China) 82541009National Natural Science Foundation of China (National Science Foundation of China) U24A20372
6 · The paper itself

Abstract

Cerebral malaria (CM) is a severe complication of Plasmodium infection, classically attributed to parasite sequestration and neuroinflammation. Here, we uncover a spleen-centered humoral autoimmune circuit that drives CM pathology. Proteomic analyses identify CD36 as a dominant host-derived antigen enriched in infected red blood cells (iRBCs), triggering anti-CD36 autoantibody production in patients with falciparum malaria. Although contributing to iRBCs clearance, these autoantibodies also target other CD36-expressing cells, thereby driving thrombocytopenia, endothelial injury, and macrophage activation, ultimately amplifying systemic inflammation. Mechanistically, Plasmodium infection recruits Ly6c

Indexed as

AutoimmunityB-LymphocytesMacrophagesMalaria, CerebralSpleenAnimalsAutoantibodiesCD36 AntigensErythrocytesFemaleGlucose Transporter Type 1HumansMalaria, FalciparumMaleMiceMice, Inbred C57BLAutoantibodiesCD36 AntigensGlucose Transporter Type 1

Identifiers

PMID42364976
PMCPMC13454142

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.