Evidence map›Paper›PMID 40589760›Full record

ArticleFrontiers in immunology2025

Hydroxychloroquine enhances efferocytosis and modulates inflammation via MerTK/Gas6 signaling in a pristane-induced lupus mouse model.

Shin-Yi Liu, Yung-Ju Yeh, Ting-Yin Xue, Fei-Hung Hsieh, Ya-Wun Wu, Meng-Zhen Wu, Wei-Jing Li, Jun-Chieh J Tsay, Shu-Yao Tsai, Chung-Ming Huang and 4 more

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Article in Frontiers in immunology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

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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

14 authors.

Shin-Yi Liu *Department of Biomedical Imaging and Radiological Science, China Medical University, Taichung, Taiwan.
Yung-Ju Yeh *Research and Development Center for Immunology, China Medical University, Taichung, Taiwan.
Ting-Yin XueResearch and Development Center for Immunology, China Medical University, Taichung, Taiwan.
Fei-Hung HsiehResearch and Development Center for Immunology, China Medical University, Taichung, Taiwan.
Ya-Wun WuResearch and Development Center for Immunology, China Medical University, Taichung, Taiwan.
Meng-Zhen WuResearch and Development Center for Immunology, China Medical University, Taichung, Taiwan.
Wei-Jing LiResearch and Development Center for Immunology, China Medical University, Taichung, Taiwan.
Jun-Chieh J TsayDivision of Pulmonary and Critical Care Medicine, New York University School of Medicine, New York, NY, United States.
Shu-Yao TsaiDepartment of Food Nutrition and Health Biotechnology, Asia University, Taichung, Taiwan.
Chung-Ming HuangDivision of Immunology and Rheumatology, Department of Internal Medicine, China Medical University Hospital, Taichung, Taiwan.
Hen-Hong ChangDepartment of Chinese Medicine, China Medical University Hospital, Taichung, Taiwan.
Hui-Chen ChenDepartment of Microbiology and Immunology, School of Medicine, China Medical University, Taichung, Taiwan.
Chun-Ping LinDepartment of Food Nutrition and Health Biotechnology, Asia University, Taichung, Taiwan.
Gregory J TsayResearch and Development Center for Immunology, China Medical University, Taichung, Taiwan.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Background: Hydroxychloroquine (HCQ) is a frontline treatment for autoimmune diseases, including rheumatoid arthritis, Sjogren's syndrome, and systemic lupus erythematosus (SLE), due to its potent immunomodulatory properties. Efferocytosis, a crucial process for tissue homeostasis by transmitting immune-suppressive signals, is frequently impaired in SLE. We hypothesized HCQ enhances efferocytosis and mediates anti-inflammatory effects. Methods: A pristane-induced lupus (PIL) mouse model was used to assess the preventive efficacy of HCQ by measuring inflammatory cytokine levels, autoantibody titers, and lupus nephritis severity. Efferocytosis in HCQ-treated macrophages was quantified following co-incubation with apoptotic cells and the expression levels of TAM family receptors post-HCQ stimulation were analyzed Results: Long-term HCQ treatment in PIL mice significantly reduced disease activity. HCQ treatment enhanced efferocytosis in RAW264.7 cells, while peritoneal macrophages from HCQ-treated mice showed increased efferocytotic capacity compare to PIL mice. Additionally, HCQ upregulated the expression of the TAM receptor MerTK and Gas6 on macrophages, restoring MerTK levels suppressed by pristane in the spleen of PIL mice. Inhibition of MerTK signaling by UNC2025 mitigated HCQ-mediated enhancements in efferocytosis and reversed the reduction in inflammatory mediators including IL-6 and IFN-α. HCQ-induced anti-inflammatory markers, such as PPARγ, LXR, and IL-10, were also alleviated upon MerTK blockade. Conclusion: This study provides robust

Indexed as

c-Mer Tyrosine KinaseHydroxychloroquineIntercellular Signaling Peptides and ProteinsLupus Erythematosus, SystemicPhagocytosisAnimalsDisease Models, AnimalEfferocytosisFemaleGrowth Arrest-Specific Protein 6InflammationMacrophagesMiceMice, Inbred C57BLRAW 264.7 CellsSignal Transductionc-Mer Tyrosine KinaseGrowth Arrest-Specific Protein 6HydroxychloroquineIntercellular Signaling Peptides and ProteinsMertk protein, mousepristaneTerpenesefferocytosisHCQinflammationMERTKSLE

Identifiers

PMID40589760
PMCPMC12206748

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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.