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Insights into IVDD pathogenesis in 2024 2024年对IVDD发病机制的见解
IF 33.7 1区 医学 Q1 RHEUMATOLOGY Pub Date : 2024-12-20 DOI: 10.1038/s41584-024-01207-4
Daisuke Sakai
Emerging research in intervertebral disc degeneration in 2024 highlights microbial, immune and inflammatory mechanisms that drive chronic low back pain. These insights pave the way for potential transformative therapies that address the root causes of intervertebral disc degeneration and could improve patient outcomes.
2024年关于椎间盘退变的新研究强调了导致慢性腰痛的微生物、免疫和炎症机制。这些见解为潜在的变革性治疗铺平了道路,这些治疗可以解决椎间盘退变的根本原因,并改善患者的预后。
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引用次数: 0
Antigen-specific immunotherapies for autoimmune disease 治疗自身免疫性疾病的抗原特异性免疫疗法
IF 33.7 1区 医学 Q1 RHEUMATOLOGY Pub Date : 2024-12-16 DOI: 10.1038/s41584-024-01201-w
Jane H. Buckner

Antigen-specific therapies have a long history in the treatment of allergy but have not been successful in autoimmunity. However, in the past 20 years, advances in the definition of the self-antigens that promote autoimmunity and the growing understanding of the mechanisms that maintain tolerance in health but fail in autoimmunity have led to antigen-specific approaches being considered for the treatment of autoimmune diseases. The core goal of each antigen-specific treatment approach is to remove the immune response that promotes autoimmunity whilst sparing protective responses. Approaches to antigen-specific therapy range from targeted deletion of autoreactive lymphocytes to tolerization of autoreactive T cells and active inhibition of autoimmune responses. Technologies such as vaccines, nanoparticles, cell-based therapies and gene editing are being harnessed to achieve these goals. Remaining challenges include the selection of the best antigen to target, modality and timing of administration of these therapies and the disease in which the therapies are used; overcoming these challenges will be vital to move antigen-specific therapies forward. Once established, antigen-specific therapy has the potential to be applied broadly in the area of autoimmunity.

抗原特异性疗法在治疗过敏症方面有着悠久的历史,但在治疗自身免疫方面却并不成功。然而,在过去 20 年中,由于对促进自身免疫的自身抗原定义的进步,以及对维持健康时的耐受性但在自身免疫中失效的机制理解的不断深入,抗原特异性疗法已被考虑用于治疗自身免疫性疾病。每种抗原特异性治疗方法的核心目标都是消除促进自身免疫的免疫反应,同时保留保护性反应。抗原特异性治疗方法包括靶向清除自体反应性淋巴细胞、耐受自体反应性 T 细胞和主动抑制自体免疫反应。目前正在利用疫苗、纳米粒子、细胞疗法和基因编辑等技术来实现这些目标。仍然存在的挑战包括选择最佳靶向抗原、给药方式和时机以及治疗的疾病;克服这些挑战对于推动抗原特异性疗法的发展至关重要。抗原特异性疗法一旦确立,就有可能广泛应用于自身免疫领域。
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引用次数: 0
Inebilizumab shows promise for IgG4-RD Inebilizumab有望治疗IgG4-RD
IF 33.7 1区 医学 Q1 RHEUMATOLOGY Pub Date : 2024-12-11 DOI: 10.1038/s41584-024-01206-5
Sarah Onuora
In a phase III trial, the CD19-targeting antibody inebilizumab was effective for the treatment of IgG4-related disease over 52 weeks.
在一项III期试验中,靶向cd19抗体inebilizumab对igg4相关疾病的治疗有效超过52周。
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引用次数: 0
Appraising the evolving landscape of protease inhibition in osteoarthritis 评价骨关节炎中蛋白酶抑制的发展前景
IF 33.7 1区 医学 Q1 RHEUMATOLOGY Pub Date : 2024-12-11 DOI: 10.1038/s41584-024-01198-2
Muhammad Farooq Rai
The role of proteases in cartilage degradation and the development of osteoarthritis is undeniable. Despite over two decades of research on protease inhibitors, however, the transition from preclinical promise to clinical success remains elusive, underscoring the urgent need to critically appraise the challenges and limitations inherent in preclinical studies.
蛋白酶在软骨降解和骨关节炎发展中的作用是不可否认的。尽管对蛋白酶抑制剂的研究已经进行了20多年,但从临床前研究到临床成功的转变仍然难以捉摸,这强调了迫切需要对临床前研究固有的挑战和局限性进行批判性评估。
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引用次数: 0
Publisher Correction: Lupus nephritis-related chronic kidney disease 出版者更正:狼疮肾炎相关的慢性肾脏疾病
IF 29.4 1区 医学 Q1 RHEUMATOLOGY Pub Date : 2024-12-09 DOI: 10.1038/s41584-024-01203-8
Julia Lichtnekert, Hans-Joachim Anders
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引用次数: 0
The ‘Treg paradox’ in inflammatory arthritis 炎性关节炎中的“Treg悖论”
IF 29.4 1区 医学 Q1 RHEUMATOLOGY Pub Date : 2024-12-09 DOI: 10.1038/s41584-024-01190-w
Julia T. Schnell, Raquel Laza Briviesca, Taehyeung Kim, Louis-Marie Charbonnier, Lauren A. Henderson, Femke van Wijk, Peter A. Nigrovic
Classic regulatory T (Treg) cells expressing CD4 and the hallmark transcription factor FOXP3 are integral to the prevention of multi-system autoimmunity. However, immune-mediated arthritis is often associated with increased numbers of Treg cells in the inflamed joints. To understand these seemingly conflicting observations, which we collectively describe as ‘the Treg paradox’, we provide an overview of Treg cell biology with a focus on Treg cell heterogeneity, function and dysfunction in arthritis. We discuss how the inflamed environment constrains the immunosuppressive activity of Treg cells while also promoting the differentiation of TH17-like Treg cell, exTreg cell (effector T cells that were formerly Treg cells), and osteoclastogenic Treg cell subsets that mediate tissue injury. We present a new framework to understand Treg cells in joint inflammation and define potential strategies for Treg cell-directed interventions in human inflammatory arthritis. In this Review, Nigrovic and colleagues examine potential mechanisms underlying the paradoxical continuation of inflammation in arthritis, despite the increased numbers of regulatory T cells in inflamed joints, and discuss the implications for regulatory T cell-targeted therapeutic interventions in inflammatory arthritis.
表达CD4和标志性转录因子FOXP3的经典调节性T (Treg)细胞是预防多系统自身免疫不可或缺的一部分。然而,免疫介导的关节炎通常与炎症关节中Treg细胞数量的增加有关。为了理解这些看似矛盾的观察结果,我们将其统称为“Treg悖论”,我们概述了Treg细胞生物学,重点关注关节炎中的Treg细胞异质性、功能和功能障碍。我们讨论了炎症环境如何限制Treg细胞的免疫抑制活性,同时也促进th17样Treg细胞、Treg细胞(以前是Treg细胞的效应T细胞)和介导组织损伤的破骨性Treg细胞亚群的分化。我们提出了一个新的框架来理解Treg细胞在关节炎症中的作用,并确定Treg细胞定向干预人类炎症性关节炎的潜在策略。
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引用次数: 0
A lung–joint axis in smokers with RA? 类风湿性关节炎吸烟者的肺关节轴?
IF 29.4 1区 医学 Q1 RHEUMATOLOGY Pub Date : 2024-12-04 DOI: 10.1038/s41584-024-01200-x
Maria Papatriantafyllou
Shared T cell clones identified in the lungs and joints of smokers with early RA.
在早期类风湿性关节炎吸烟者的肺和关节中发现的共享T细胞克隆。
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引用次数: 0
Impaired adipocyte-mediated regulation of fibroblasts in inflammatory arthritis 炎性关节炎中脂肪细胞介导的成纤维细胞调节受损
IF 29.4 1区 医学 Q1 RHEUMATOLOGY Pub Date : 2024-12-03 DOI: 10.1038/s41584-024-01202-9
Holly Webster
A study reports that adipocytes can regulate the metabolism of fibroblasts in the healthy synovium via cortisol, but in inflammatory arthritis adiposity is lost and fibroblasts become pathogenic.
一项研究报道,脂肪细胞可以通过皮质醇调节健康滑膜中成纤维细胞的代谢,但在炎症性关节炎中,脂肪丢失,成纤维细胞成为致病性的。
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引用次数: 0
Wnt-induced IGF1 drives OA wnt诱导的IGF1驱动OA
IF 29.4 1区 医学 Q1 RHEUMATOLOGY Pub Date : 2024-12-03 DOI: 10.1038/s41584-024-01199-1
Sarah Onuora
New research suggests that insulin-like growth factor 1 is an important contributor to Wnt-induced joint damage, and that its suppression could represent a promising therapeutic strategy for osteoarthritis.
新的研究表明,胰岛素样生长因子1是wnt诱导的关节损伤的重要因素,抑制其可能是骨关节炎的一种有希望的治疗策略。
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引用次数: 0
A subset of ITGA5+ synovial fibroblasts alter the inflammatory niche in RA ITGA5+滑膜成纤维细胞亚群改变类风湿关节炎的炎症生态位
IF 29.4 1区 医学 Q1 RHEUMATOLOGY Pub Date : 2024-12-03 DOI: 10.1038/s41584-024-01197-3
Holly Webster
The release of TGFβ by a subset of ITGA5+ synovial fibroblasts can promote the differentiation of pathogenic PD-1hiCXCL13+ T cells in RA, altering the inflammatory niche.
ITGA5+滑膜成纤维细胞亚群释放TGFβ可促进RA中致病性PD-1hiCXCL13+ T细胞的分化,改变炎症生态位。
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引用次数: 0
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Nature Reviews Rheumatology
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