Evidence map›Paper›PMID 42061907›Full record

ArticleBriefings in bioinformatics2026

A causal glycerophospholipid-IL-18R1-CD9 axis connects lipid metabolism and T-cell activation in atopic dermatitis.

Ping-An Zhang, Jie-Lin Wang, Run-Dong Qin, Xiao-Nan Song, Ren-Ke Mo, Mei-Hua Dong, Xuan-Yu Pan, Jing Liu, Wan-Jun Wang, Shuo Chen and 1 more

Abstract read
In one paragraph

Article in Briefings in bioinformatics, 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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0cells of the map it votes in
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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3 · Its place in the literature

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4 · The record

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5 · Who and what money

Authors and funding

11 authors.

Ping-An Zhang *State Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, Department of Allergy and Clinical Immunology, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiangxi Rd, Guangzhou, Guangdong 510120, China.ORCID 0009-0002-5897-8100
Jie-Lin Wang *Department of Obstetrics and Gynecology, Department of Gynecologic Oncology Research Office, Guangzhou Key Laboratory of Targeted Therapy for Gynecologic Oncology, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, The Third Affiliated Hospital, Guangzhou Medical University, No. 63 Duobao Road, Liwan District, Guangzhou, Guangdong 510150, China.ORCID 0009-0006-2088-9099
Run-Dong QinState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, Department of Allergy and Clinical Immunology, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiangxi Rd, Guangzhou, Guangdong 510120, China.ORCID 0000-0001-8067-6307
Xiao-Nan SongState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, Department of Allergy and Clinical Immunology, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiangxi Rd, Guangzhou, Guangdong 510120, China.ORCID 0009-0007-5195-5279
Ren-Ke MoState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, Department of Allergy and Clinical Immunology, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiangxi Rd, Guangzhou, Guangdong 510120, China.ORCID 0009-0008-9031-7074
Mei-Hua DongState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, Department of Allergy and Clinical Immunology, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiangxi Rd, Guangzhou, Guangdong 510120, China.ORCID 0009-0000-5132-9197
Xuan-Yu PanState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, Department of Allergy and Clinical Immunology, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiangxi Rd, Guangzhou, Guangdong 510120, China.ORCID 0009-0008-3999-5128
Jing LiuState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, Department of Allergy and Clinical Immunology, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiangxi Rd, Guangzhou, Guangdong 510120, China.
Wan-Jun WangState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, Department of Allergy and Clinical Immunology, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiangxi Rd, Guangzhou, Guangdong 510120, China.
Shuo ChenDepartment of Obstetrics and Gynecology, Department of Gynecologic Oncology Research Office, Guangzhou Key Laboratory of Targeted Therapy for Gynecologic Oncology, Guangdong Provincial Key Laboratory of Major Obstetric Diseases, Guangdong Provincial Clinical Research Center for Obstetrics and Gynecology, Guangdong-Hong Kong-Macao Greater Bay Area Higher Education Joint Laboratory of Maternal-Fetal Medicine, The Third Affiliated Hospital, Guangzhou Medical University, No. 63 Duobao Road, Liwan District, Guangzhou, Guangdong 510150, China.ORCID 0000-0002-5122-3656
Jing LiState Key Laboratory of Respiratory Disease, National Clinical Research Center for Respiratory Disease, Guangzhou Institute of Respiratory Health, Department of Allergy and Clinical Immunology, The First Affiliated Hospital of Guangzhou Medical University, 151 Yanjiangxi Rd, Guangzhou, Guangdong 510120, China.ORCID 0000-0002-6459-7470

Funding

National Natural Science Foundation of China 82161138020Non-communicable Chronic Diseases-National Science and Technology Major Project 2024ZD0529900
6 · The paper itself

Abstract

Atopic dermatitis (AD) involves complex metabolic-immune dysregulation, but the molecular links remain unclear. This study integrates a multilevel analytical framework to systematically investigate the metabolic-immune crosstalk in AD. Using linkage disequilibrium score regression and a two-step Mendelian randomization approach, we established genetic correlations and inferred causal relationships between plasma metabolites and inflammatory proteins, identifying 1-palmitoyl-2-arachidonoyl-GPC (PA-GPC) as a protective metabolite that exerts its effect primarily through downregulation of interleukin-18 receptor 1 (IL-18R1). Integration of single-cell transcriptomic data further revealed elevated IL-18R1 expression in T cells within the AD microenvironment and enabled stratification of T cells based on PA-GPC-associated metabolic activity, identifying 33 differentially expressed genes. Subsequent least absolute shrinkage and selection operator (LASSO) regression, combined with machine learning models and SHapley Additive exPlanations analysis, consistently prioritized CD9 as a key regulator. Functional validation showed that PA-GPC attenuates tumor necrosis factor-alpha (TNF-α)/interferon-gamma (IFN-γ)-induced inflammatory responses in human immortalized keratinocyte (HaCaT) cells and suppresses Th2 cytokine production in T cells. IL-18R1 knockdown reduced CD9 expression and Th2 cytokine production in T cells, whereas CD9 knockdown did not affect IL-18R1 expression, indicating that IL-18R1 acts upstream of CD9. Moreover, CD9 knockdown impaired T-cell viability, activation, and Th2 cytokine production. Collectively, these findings characterize metabolic-immune crosstalk in AD and identify a PA-GPC-IL-18R1-CD9 regulatory axis with potential therapeutic implications.

Indexed as

Dermatitis, AtopicGlycerophospholipidsInterleukin-18 Receptor alpha SubunitLipid MetabolismLymphocyte ActivationTetraspanin 29T-LymphocytesHumansCD9 protein, humanGlycerophospholipidsIL18R1 protein, humanInterleukin-18 Receptor alpha SubunitTetraspanin 29atopic dermatitisCD9IL-18R1inflammatory proteinsMendelian randomization analysismetabolomics

Identifiers

PMID42061907
PMCPMC13132603

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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.