A triple-targeting “nano-brake” remodeling the impaired immune microenvironment in skin lesions for psoriasis treatment

Psoriasis, a prevalent immune-mediated chronic inflammatory skin ailment, has been linked to heightened oxidative stress and compromised immune tolerance. Immune checkpoint pathways, particularly the programmed cell death-1 (PD-1)/programmed cell death-ligand 1 (PD-L1) signaling axis, are instrument...

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Main Authors: Ruijie Chen, Baiqun Duan, Shize Li, Yixuan Zhu, Zihao Huang, Dingchao Shen, Zhanzheng Ye, Yuqi Yan, Chenyu Qiu, Haoxiong Guan, Yinsha Yao, Jie Dong, Fugen Wu, Xinyu Jiang, Xianbao Shi, Longfa Kou
Format: Article
Language:English
Published: Elsevier 2025-06-01
Series:Materials Today Bio
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Online Access:http://www.sciencedirect.com/science/article/pii/S2590006425004351
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author Ruijie Chen
Baiqun Duan
Shize Li
Yixuan Zhu
Zihao Huang
Dingchao Shen
Zhanzheng Ye
Yuqi Yan
Chenyu Qiu
Haoxiong Guan
Yinsha Yao
Jie Dong
Fugen Wu
Xinyu Jiang
Xianbao Shi
Longfa Kou
author_facet Ruijie Chen
Baiqun Duan
Shize Li
Yixuan Zhu
Zihao Huang
Dingchao Shen
Zhanzheng Ye
Yuqi Yan
Chenyu Qiu
Haoxiong Guan
Yinsha Yao
Jie Dong
Fugen Wu
Xinyu Jiang
Xianbao Shi
Longfa Kou
author_sort Ruijie Chen
collection DOAJ
description Psoriasis, a prevalent immune-mediated chronic inflammatory skin ailment, has been linked to heightened oxidative stress and compromised immune tolerance. Immune checkpoint pathways, particularly the programmed cell death-1 (PD-1)/programmed cell death-ligand 1 (PD-L1) signaling axis, are instrumental in establishing and sustaining self-tolerance and regulating immune responses. Augmenting PD-1/PD-L1 interaction holds promise for curtailing the proliferation and activation of infiltrating T cells and curbing the release of inflammatory cytokines, thereby mitigating psoriasis induced by impaired immune tolerance. Consequently, neutralizing the surplus reactive oxygen species (ROS) in the affected skin and revitalizing local immune tolerance could represent a beneficial approach to psoriasis treatment. In light of these insights, this study introduced a bilirubin-based nanoparticle cloaked in IFN-γ-stimulated macrophage membrane (designated as IMφm@GBn or ''nano-brake''). Treatment with IFN-γ conferred the macrophage membrane with heightened expression of pro-inflammatory cytokine receptor and PD-L1. As a result, the engineered IMφm@GBn not only scavenged excessive ROS in psoriatic lesions but crucially also absorbed a wide spectrum of pro-inflammatory cytokines. Furthermore, it inhibited the proliferation and activation of infiltrating T cells through augmented PD-1/PD-L1 interactions, thereby rebalancing the Th17/Treg ratio. In an in vivo psoriasis mouse model, the ''nano-brake'' was locally and accurately delivered to the dermis via microneedle, orchestrating the immune microenvironment of psoriasis and mitigating autoimmune damage linked to impaired immune tolerance. This approach significantly enhanced the therapeutic efficacy in ameliorating psoriasis-associated symptoms. This study sets an illuminating precedent for cell membrane-based biomimetic nano-formulations, holding broad implications for psoriasis treatment through multi-pronged immunomodulation.
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spelling doaj-art-37f739e2056e4cc99daa13768630f88f2025-08-20T02:25:44ZengElsevierMaterials Today Bio2590-00642025-06-013210187510.1016/j.mtbio.2025.101875A triple-targeting “nano-brake” remodeling the impaired immune microenvironment in skin lesions for psoriasis treatmentRuijie Chen0Baiqun Duan1Shize Li2Yixuan Zhu3Zihao Huang4Dingchao Shen5Zhanzheng Ye6Yuqi Yan7Chenyu Qiu8Haoxiong Guan9Yinsha Yao10Jie Dong11Fugen Wu12Xinyu Jiang13Xianbao Shi14Longfa Kou15Wenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, ChinaDepartment of Pharmacy, The Second Affiliated Hospital of Jiaxing University, Jiaxing, ChinaWenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, ChinaWenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China; School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, 325035, China; Key Laboratory of Structural Malformations in Children of Zhejiang Province, Wenzhou, 325027, ChinaWenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China; School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, 325035, China; Key Laboratory of Structural Malformations in Children of Zhejiang Province, Wenzhou, 325027, ChinaWenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China; Key Laboratory of Structural Malformations in Children of Zhejiang Province, Wenzhou, 325027, ChinaWenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China; Key Laboratory of Structural Malformations in Children of Zhejiang Province, Wenzhou, 325027, ChinaWenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China; Key Laboratory of Structural Malformations in Children of Zhejiang Province, Wenzhou, 325027, ChinaWenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China; Key Laboratory of Structural Malformations in Children of Zhejiang Province, Wenzhou, 325027, ChinaWenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, ChinaWenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China; School of Pharmaceutical Sciences, Wenzhou Medical University, Wenzhou, 325035, ChinaWenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, ChinaDepartment of Pediatric, The First People's Hospital of Wenling, Taizhou, ChinaWenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China; Key Laboratory of Structural Malformations in Children of Zhejiang Province, Wenzhou, 325027, ChinaDepartment of Pharmacy, The First Affiliated Hospital of Jinzhou Medical University, Jinzhou, ChinaWenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China; Key Laboratory of Structural Malformations in Children of Zhejiang Province, Wenzhou, 325027, China; Corresponding author. Wenzhou Municipal Key Laboratory of Pediatric Pharmacy, Department of Pharmacy, The Second Affiliated Hospital and Yuying Children's Hospital of Wenzhou Medical University, Wenzhou, 325027, China.Psoriasis, a prevalent immune-mediated chronic inflammatory skin ailment, has been linked to heightened oxidative stress and compromised immune tolerance. Immune checkpoint pathways, particularly the programmed cell death-1 (PD-1)/programmed cell death-ligand 1 (PD-L1) signaling axis, are instrumental in establishing and sustaining self-tolerance and regulating immune responses. Augmenting PD-1/PD-L1 interaction holds promise for curtailing the proliferation and activation of infiltrating T cells and curbing the release of inflammatory cytokines, thereby mitigating psoriasis induced by impaired immune tolerance. Consequently, neutralizing the surplus reactive oxygen species (ROS) in the affected skin and revitalizing local immune tolerance could represent a beneficial approach to psoriasis treatment. In light of these insights, this study introduced a bilirubin-based nanoparticle cloaked in IFN-γ-stimulated macrophage membrane (designated as IMφm@GBn or ''nano-brake''). Treatment with IFN-γ conferred the macrophage membrane with heightened expression of pro-inflammatory cytokine receptor and PD-L1. As a result, the engineered IMφm@GBn not only scavenged excessive ROS in psoriatic lesions but crucially also absorbed a wide spectrum of pro-inflammatory cytokines. Furthermore, it inhibited the proliferation and activation of infiltrating T cells through augmented PD-1/PD-L1 interactions, thereby rebalancing the Th17/Treg ratio. In an in vivo psoriasis mouse model, the ''nano-brake'' was locally and accurately delivered to the dermis via microneedle, orchestrating the immune microenvironment of psoriasis and mitigating autoimmune damage linked to impaired immune tolerance. This approach significantly enhanced the therapeutic efficacy in ameliorating psoriasis-associated symptoms. This study sets an illuminating precedent for cell membrane-based biomimetic nano-formulations, holding broad implications for psoriasis treatment through multi-pronged immunomodulation.http://www.sciencedirect.com/science/article/pii/S2590006425004351PsoriasisBilirubinROSPD-1/PDL-1Th17/Treg
spellingShingle Ruijie Chen
Baiqun Duan
Shize Li
Yixuan Zhu
Zihao Huang
Dingchao Shen
Zhanzheng Ye
Yuqi Yan
Chenyu Qiu
Haoxiong Guan
Yinsha Yao
Jie Dong
Fugen Wu
Xinyu Jiang
Xianbao Shi
Longfa Kou
A triple-targeting “nano-brake” remodeling the impaired immune microenvironment in skin lesions for psoriasis treatment
Materials Today Bio
Psoriasis
Bilirubin
ROS
PD-1/PDL-1
Th17/Treg
title A triple-targeting “nano-brake” remodeling the impaired immune microenvironment in skin lesions for psoriasis treatment
title_full A triple-targeting “nano-brake” remodeling the impaired immune microenvironment in skin lesions for psoriasis treatment
title_fullStr A triple-targeting “nano-brake” remodeling the impaired immune microenvironment in skin lesions for psoriasis treatment
title_full_unstemmed A triple-targeting “nano-brake” remodeling the impaired immune microenvironment in skin lesions for psoriasis treatment
title_short A triple-targeting “nano-brake” remodeling the impaired immune microenvironment in skin lesions for psoriasis treatment
title_sort triple targeting nano brake remodeling the impaired immune microenvironment in skin lesions for psoriasis treatment
topic Psoriasis
Bilirubin
ROS
PD-1/PDL-1
Th17/Treg
url http://www.sciencedirect.com/science/article/pii/S2590006425004351
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