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

BackgroundHydroxychloroquine (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 immu...

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Main Authors: 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, Hen-Hong Chang, Hui-Chen Chen, Chun-Ping Lin, Gregory J. Tsay
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Language:English
Published: Frontiers Media S.A. 2025-06-01
Series:Frontiers in Immunology
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Online Access:https://www.frontiersin.org/articles/10.3389/fimmu.2025.1524315/full
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author Shin-Yi Liu
Shin-Yi Liu
Shin-Yi Liu
Yung-Ju Yeh
Yung-Ju Yeh
Ting-Yin Xue
Ting-Yin Xue
Fei-Hung Hsieh
Fei-Hung Hsieh
Ya-Wun Wu
Ya-Wun Wu
Meng-Zhen Wu
Meng-Zhen Wu
Wei-Jing Li
Wei-Jing Li
Jun-Chieh J. Tsay
Jun-Chieh J. Tsay
Shu-Yao Tsai
Chung-Ming Huang
Chung-Ming Huang
Hen-Hong Chang
Hen-Hong Chang
Hui-Chen Chen
Chun-Ping Lin
Gregory J. Tsay
Gregory J. Tsay
Gregory J. Tsay
author_facet Shin-Yi Liu
Shin-Yi Liu
Shin-Yi Liu
Yung-Ju Yeh
Yung-Ju Yeh
Ting-Yin Xue
Ting-Yin Xue
Fei-Hung Hsieh
Fei-Hung Hsieh
Ya-Wun Wu
Ya-Wun Wu
Meng-Zhen Wu
Meng-Zhen Wu
Wei-Jing Li
Wei-Jing Li
Jun-Chieh J. Tsay
Jun-Chieh J. Tsay
Shu-Yao Tsai
Chung-Ming Huang
Chung-Ming Huang
Hen-Hong Chang
Hen-Hong Chang
Hui-Chen Chen
Chun-Ping Lin
Gregory J. Tsay
Gregory J. Tsay
Gregory J. Tsay
author_sort Shin-Yi Liu
collection DOAJ
description BackgroundHydroxychloroquine (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.MethodsA 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 in vitro and in vivo. The role of MerTK on HCQ-modulated inflammation was revealed by MerTK inhibitor UNC2025.ResultsLong-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.ConclusionThis study provides robust in vitro and in vivo evidence that HCQ promotes macrophage efferocytosis and anti-inflammatory reprogramming via MerTK/Gas6 signaling, offering insights into potential therapeutic mechanisms in SLE management.
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spelling doaj-art-1ae774fb19e341d9b521b8b7b11bc0332025-08-20T02:39:52ZengFrontiers Media S.A.Frontiers in Immunology1664-32242025-06-011610.3389/fimmu.2025.15243151524315Hydroxychloroquine enhances efferocytosis and modulates inflammation via MerTK/Gas6 signaling in a pristane-induced lupus mouse modelShin-Yi Liu0Shin-Yi Liu1Shin-Yi Liu2Yung-Ju Yeh3Yung-Ju Yeh4Ting-Yin Xue5Ting-Yin Xue6Fei-Hung Hsieh7Fei-Hung Hsieh8Ya-Wun Wu9Ya-Wun Wu10Meng-Zhen Wu11Meng-Zhen Wu12Wei-Jing Li13Wei-Jing Li14Jun-Chieh J. Tsay15Jun-Chieh J. Tsay16Shu-Yao Tsai17Chung-Ming Huang18Chung-Ming Huang19Hen-Hong Chang20Hen-Hong Chang21Hui-Chen Chen22Chun-Ping Lin23Gregory J. Tsay24Gregory J. Tsay25Gregory J. Tsay26Department of Biomedical Imaging and Radiological Science, China Medical University, Taichung, TaiwanGraduate Institute of Biomedical Sciences, China Medical University, Taichung, TaiwanResearch and Development Center for Immunology, China Medical University, Taichung, TaiwanResearch and Development Center for Immunology, China Medical University, Taichung, TaiwanDivision of Immunology and Rheumatology, Department of Internal Medicine, China Medical University Hospital, Taichung, TaiwanResearch and Development Center for Immunology, China Medical University, Taichung, TaiwanDivision of Immunology and Rheumatology, Department of Internal Medicine, China Medical University Hospital, Taichung, TaiwanResearch and Development Center for Immunology, China Medical University, Taichung, TaiwanDivision of Immunology and Rheumatology, Department of Internal Medicine, China Medical University Hospital, Taichung, TaiwanResearch and Development Center for Immunology, China Medical University, Taichung, TaiwanDivision of Immunology and Rheumatology, Department of Internal Medicine, China Medical University Hospital, Taichung, TaiwanResearch and Development Center for Immunology, China Medical University, Taichung, TaiwanDivision of Immunology and Rheumatology, Department of Internal Medicine, China Medical University Hospital, Taichung, TaiwanResearch and Development Center for Immunology, China Medical University, Taichung, TaiwanDivision of Immunology and Rheumatology, Department of Internal Medicine, China Medical University Hospital, Taichung, TaiwanDivision of Pulmonary and Critical Care Medicine, New York University School of Medicine, New York, NY, United StatesDivision of Pulmonary and Critical Care Medicine, Veterans Administration (VA) New York Harbor Healthcare System, New York, NY, United StatesDepartment of Food Nutrition and Health Biotechnology, Asia University, Taichung, TaiwanDivision of Immunology and Rheumatology, Department of Internal Medicine, China Medical University Hospital, Taichung, TaiwanCollege of Medicine, China Medical University, Taichung, TaiwanDepartment of Chinese Medicine, China Medical University Hospital, Taichung, Taiwan0Graduate Institute of Integrated Medicine, Graduate Institute of Acupuncture Science, College of Chinese Medicine, China Medical University, Taichung, Taiwan1Department of Microbiology and Immunology, School of Medicine, China Medical University, Taichung, TaiwanDepartment of Food Nutrition and Health Biotechnology, Asia University, Taichung, TaiwanResearch and Development Center for Immunology, China Medical University, Taichung, TaiwanDivision of Immunology and Rheumatology, Department of Internal Medicine, China Medical University Hospital, Taichung, TaiwanCollege of Medicine, China Medical University, Taichung, TaiwanBackgroundHydroxychloroquine (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.MethodsA 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 in vitro and in vivo. The role of MerTK on HCQ-modulated inflammation was revealed by MerTK inhibitor UNC2025.ResultsLong-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.ConclusionThis study provides robust in vitro and in vivo evidence that HCQ promotes macrophage efferocytosis and anti-inflammatory reprogramming via MerTK/Gas6 signaling, offering insights into potential therapeutic mechanisms in SLE management.https://www.frontiersin.org/articles/10.3389/fimmu.2025.1524315/fullHCQefferocytosisMERTKinflammationSLE
spellingShingle Shin-Yi Liu
Shin-Yi Liu
Shin-Yi Liu
Yung-Ju Yeh
Yung-Ju Yeh
Ting-Yin Xue
Ting-Yin Xue
Fei-Hung Hsieh
Fei-Hung Hsieh
Ya-Wun Wu
Ya-Wun Wu
Meng-Zhen Wu
Meng-Zhen Wu
Wei-Jing Li
Wei-Jing Li
Jun-Chieh J. Tsay
Jun-Chieh J. Tsay
Shu-Yao Tsai
Chung-Ming Huang
Chung-Ming Huang
Hen-Hong Chang
Hen-Hong Chang
Hui-Chen Chen
Chun-Ping Lin
Gregory J. Tsay
Gregory J. Tsay
Gregory J. Tsay
Hydroxychloroquine enhances efferocytosis and modulates inflammation via MerTK/Gas6 signaling in a pristane-induced lupus mouse model
Frontiers in Immunology
HCQ
efferocytosis
MERTK
inflammation
SLE
title Hydroxychloroquine enhances efferocytosis and modulates inflammation via MerTK/Gas6 signaling in a pristane-induced lupus mouse model
title_full Hydroxychloroquine enhances efferocytosis and modulates inflammation via MerTK/Gas6 signaling in a pristane-induced lupus mouse model
title_fullStr Hydroxychloroquine enhances efferocytosis and modulates inflammation via MerTK/Gas6 signaling in a pristane-induced lupus mouse model
title_full_unstemmed Hydroxychloroquine enhances efferocytosis and modulates inflammation via MerTK/Gas6 signaling in a pristane-induced lupus mouse model
title_short Hydroxychloroquine enhances efferocytosis and modulates inflammation via MerTK/Gas6 signaling in a pristane-induced lupus mouse model
title_sort hydroxychloroquine enhances efferocytosis and modulates inflammation via mertk gas6 signaling in a pristane induced lupus mouse model
topic HCQ
efferocytosis
MERTK
inflammation
SLE
url https://www.frontiersin.org/articles/10.3389/fimmu.2025.1524315/full
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