Targeting formyl peptide receptor 2 to suppress neuroinflammation in neuromyelitis optica spectrum disorder
文献类型：期刊论文
| 作者 | Qi, Caiyun4; Hao, Hongying; Zhang, Wei4; Fu, Yiwei; Han, Yali; Li, Jinyi; Chen, Lixiang; Cui, Guiyun4; Liu, Qing; Li, Yuan5 |
| 刊名 | THERANOSTICS
 |
| 出版日期 | 2025 |
| 卷号 | 15期号:10页码:4495-4506 |
| 关键词 | FPR2/mFpr2 demyelination neuroinflammation neuromyelitis optica spectrum disorder |
| ISSN号 | 1838-7640 |
| DOI | 10.7150/thno.107303 |
| 通讯作者 | Wang, Ming-Wei(mwwang@simm.ac.cn) ; Liu, Qiang(qliu@tmu.edu.cn) |
| 英文摘要 | Background: Neuromyelitis optica spectrum disorder (NMOSD) is an antibody-mediated neurological inflammatory disease. As a G protein-coupled receptor, formyl peptide receptor 2 (FPR2) orchestrates innate and adaptive immunity. Yet the precise role of FPR2 in neuroinflammation is poorly understood. Methods: Peripheral blood samples were collected from patients with NMOSD and healthy controls. Single-cell RNA sequencing (scRNA-seq) and flow cytometry were employed to assess the expression of FPR2 in immune cell subsets. We used a mouse model of NMOSD to examine the therapeutic potential and underlying immune mechanisms of an FPR2 antagonist Quin-C7. MRI and immunostaining were performed to quantify central nervous system injury. Results: ScRNA-seq and flow cytometry analyses revealed that FPR2 was expressed in various myeloid and lymphoid cell types in patients with NMOSD and a mouse model of NMOSD. In NMOSD mice, mouse formyl peptide receptor 2 (mFpr2) was mainly upregulated in microglia. Administration of Quin-C7 led to reduced brain lesion volume, astrocyte loss and demyelination in NMOSD mice. Further, FPR2 antagonism reduced the inflammatory activity of microglia and lymphocyte infiltration into the brain. Notably, depletion of microglia using a CSF1R inhibitor diminished the protective effects of FPR2 antagonism, suggesting that microglia contribute to the benefit of FPR2 antagonism in NMOSD. In contrast, genetic deficiency of T and B cells or antibody depletion of NK cells did not affect the benefit of FPR2 antagonism. Conclusion: Collectively, our findings revealed a previously unrecognized role of FPR2/mFpr2 in control of microglia activity during neuroinflammation, implying that FPR2 antagonism may serve as a viable therapeutic approach to restrict detrimental neuroinflammation and warrant further investigation. |
| 资助项目 | National Key R&D Program of China STI2030-Major Projects[2021ZD0202400] ; National Natural Science Foundation of China[82488301] ; National Natural Science Foundation of China[82301522] ; National Natural Science Foundation of China[82225015] ; National Natural Science Foundation of China[82171284] ; National Natural Science Foundation of China[82301495] ; National Natural Science Foundation of China[82201498] ; National Natural Science Foundation of China[82372651] ; National Natural Science Foundation of China[82271378] ; National Natural Science Foundation of China[82273961] ; National Natural Science Foundation of China[82073904] ; National Natural Science Foundation of China[81872915] ; Tianjin Municipal Science and Technology Bureau[22JCQNJC00500] ; Tianjin Municipal Education Commission[2021KJ215] ; Tianjin Municipal Education Commission[2021ZD035] ; National Postdoctoral Program for Innovative Talents[BX20240097] ; China Postdoctoral Science Foundation[2024M750652] ; Tianjin Municipal Health Commission Science and Technology Project[TJWJ2023QN011] ; Tianjin Municipal Health Commission Science and Technology Project[TJWJ2024XK002] |
| WOS研究方向 | Research & Experimental Medicine |
| 语种 | 英语 |
| WOS记录号 | WOS:001473295700014 |
| 出版者 | IVYSPRING INT PUBL |
| 源URL | [http://119.78.100.183/handle/2S10ELR8/317563]  |
| 专题 | 中国科学院上海药物研究所 |
| 通讯作者 | Wang, Ming-Wei; Liu, Qiang |
| 作者单位 | 1.Fudan Univ, Sch Basic Med Sci, Dept Pharmacol, Shanghai 200032, Peoples R China 2.Shanghai Jiao Tong Univ, Res Ctr Med Struct Biol, Natl Res Ctr Translat Med Shanghai, State Key Lab Med Genom,Ruijin Hosp,Sch Med, Shanghai 200025, Peoples R China 3.Hainan Med Univ, Engn Res Ctr Trop Med Innovat & Transformat, Sch Pharm, Minist Educ, Haikou 570228, Peoples R China 4.Xuzhou Med Univ, Affiliated Hosp, Parkinsons Dis Ctr, Dept Neurol, Xuzhou, Peoples R China 5.Tianjin Med Univ, Int Joint Lab Ocular Dis, Haihe Lab Cell Ecosyst, Lab Postneuroinjury Neurorepair & Regenerat Cent N, Tianjin 300052, Peoples R China 6.Chinese Acad Sci, Shanghai Inst Mat Med, Natl Ctr Drug Screening, Shanghai 201203, Peoples R China 7.Res Ctr Deepsea Bioresources, Sanya 572025, Peoples R China |
| 推荐引用方式 GB/T 7714 | Qi, Caiyun,Hao, Hongying,Zhang, Wei,et al. Targeting formyl peptide receptor 2 to suppress neuroinflammation in neuromyelitis optica spectrum disorder[J]. THERANOSTICS,2025,15(10):4495-4506. |
| APA | Qi, Caiyun.,Hao, Hongying.,Zhang, Wei.,Fu, Yiwei.,Han, Yali.,...&Liu, Qiang.(2025).Targeting formyl peptide receptor 2 to suppress neuroinflammation in neuromyelitis optica spectrum disorder.THERANOSTICS,15(10),4495-4506. |
| MLA | Qi, Caiyun,et al."Targeting formyl peptide receptor 2 to suppress neuroinflammation in neuromyelitis optica spectrum disorder".THERANOSTICS 15.10(2025):4495-4506. |
入库方式： OAI收割
来源：上海药物研究所
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