高迁移率族蛋白盒1作为类风湿关节炎中不依赖肿瘤坏死因子的治疗靶点
High mobility group box-1 protein as a tumor necrosis factor-independent therapeutic target in rheumatoid arthritis.
作者信息
Goldstein Richard S
出版信息
Arthritis Res Ther. 2008;10(3):111. doi: 10.1186/ar2427. Epub 2008 Jun 2.
Abstract
Rheumatoid arthritis (RA) remains a prevalent disease worldwide that causes significant morbidity and mortality despite recent therapeutics. High mobility group box-1 (HMGB1) protein, originally appreciated as an intranuclear DNA binding protein, has been implicated as an integral mediator in the pathogenesis of animal arthritides and RA disease in humans. Our current understanding of HMGB1 has promoted the development of targeting therapies that have improved outcomes in animal models of inflammation. In the previous issue of Arthritis Research & Therapy, Sundberg and colleagues address, for the first time in a prospective cohort study, whether HMGB1 expression is dependent upon tumor necrosis factor activity in patients with RA.
摘要
类风湿性关节炎（RA）在全球范围内仍然是一种普遍存在的疾病，尽管有了最新的治疗方法，但仍会导致严重的发病率和死亡率。高迁移率族蛋白B1（HMGB1）最初被认为是一种核内DNA结合蛋白，现已被认为是动物关节炎和人类RA疾病发病机制中的一个重要介质。我们目前对HMGB1的理解推动了靶向治疗的发展，这些治疗在炎症动物模型中改善了治疗效果。在上一期的《关节炎研究与治疗》中，桑德伯格及其同事在一项前瞻性队列研究中首次探讨了RA患者中HMGB1的表达是否依赖于肿瘤坏死因子活性。
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