释放治疗潜力:用纤维蛋白原样蛋白 1 (FGL1) 靶向淋巴细胞活化基因-3 (LAG-3) 治疗系统性红斑狼疮

IF 4.7 Q2 IMMUNOLOGY Journal of Translational Autoimmunity Pub Date : 2024-07-27 DOI:10.1016/j.jtauto.2024.100249
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引用次数: 0

摘要

系统性红斑狼疮(SLE)是一种影响多个系统的自身免疫性疾病。治疗这种疾病的重点主要是抑制炎症和免疫抑制。因此,靶向治疗已成为一种主流方法。目前,在系统性红斑狼疮的治疗中,寻找高灵敏度和特异性有效靶点的工作取得了显著的进展。淋巴细胞活化基因-3(LAG-3)是一种重要的抑制受体,它能与 pMHC-II 结合,从而有效抑制自身免疫反应。纤维蛋白原样蛋白 1(FGL1)是 LAG-3 的主要免疫抑制配体,它们的联合作用显示出强大的免疫抑制效果。这一错综复杂的机制为通过 FGL1 靶向 LAG-3 治疗系统性红斑狼疮铺平了道路。这项研究全面总结了 LAG-3 在系统性红斑狼疮发病机制中的作用,阐明了利用 FGL1 作为系统性红斑狼疮治疗方法的可行性。它引入了一个新的治疗靶点,为系统性红斑狼疮的临床治疗开辟了新的治疗途径。
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Unlocking therapeutic potential: Targeting lymphocyte activation Gene-3 (LAG-3) with fibrinogen-like protein 1 (FGL1) in systemic lupus erythematosus

Systemic lupus erythematosus (SLE) represents an autoimmune disorder that affects multiple systems. In the treatment of this condition, the focus primarily revolves around inflammation suppression and immunosuppression. Consequently, targeted therapy has emerged as a prevailing approach. Currently, the quest for highly sensitive and specifically effective targets has gained significant momentum in the context of SLE treatment. Lymphocyte activation gene-3 (LAG-3) stands out as a crucial inhibitory receptor that binds to pMHC-II, thereby effectively dampening autoimmune responses. Fibrinogen-like protein 1 (FGL1) serves as the principal immunosuppressive ligand for LAG-3, and their combined action demonstrates a potent immunosuppressive effect. This intricate mechanism paves the way for potential SLE treatment by targeting LAG-3 with FGL1. This work provides a comprehensive summary of LAG-3's role in the pathogenesis of SLE and elucidates the feasibility of leveraging FGL1 as a therapeutic approach for SLE management. It introduces a novel therapeutic target and opens up new avenues of therapeutic consideration in the clinical context of SLE treatment.

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来源期刊
Journal of Translational Autoimmunity
Journal of Translational Autoimmunity Medicine-Immunology and Allergy
CiteScore
7.80
自引率
2.60%
发文量
33
审稿时长
55 days
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