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青少年特发性关节炎中的热休克蛋白:理解缓解性关节炎的关键及免疫治疗的候选抗原

Heat shock proteins in juvenile idiopathic arthritis: keys for understanding remitting arthritis and candidate antigens for immune therapy.

作者信息

Prakken Berent, Kuis Wietse, van Eden Willem, Albani Salvatore

机构信息

Department of Pediatric Immunology, University Medical Center Utrecht, University Hospital for Children and Youth, PO Box 85090, Utrecht 3508 AB, The Netherlands.

出版信息

Curr Rheumatol Rep. 2002 Dec;4(6):466-73. doi: 10.1007/s11926-002-0052-7.

DOI:10.1007/s11926-002-0052-7
PMID:12427360
Abstract

Juvenile idiopathic arthritis (JIA) is in a majority of the cases of self-limiting, and sometimes even a self-remitting, disease. A growing amount of data suggests that active T cell regulation determines, at least partly, the clinical outcome of JIA. In experimental models of arthritis, a group of highly conserved microbial proteins, heat shock proteins (hsps), can be used to effectively prevent and treat arthritis. This protection is mediated through the induction of cross-reactive T cell responses to self-hsps. In JIA, naturally occurring T cell immune responses to hsps are associated with disease remission in restricted oligoarticular JIA. Moreover, those responses are associated with the induction of T cells with a regulatory phenotype. Taken together, these data imply that immune modulation with hsps can be an effective way to restore natural occurring T cell responses, and, thus, treat JIA and rheumatoid arthritis.

摘要

青少年特发性关节炎(JIA)在大多数情况下是一种自限性疾病,甚至有时会自行缓解。越来越多的数据表明,活跃的T细胞调节至少部分决定了JIA的临床结局。在关节炎的实验模型中,一组高度保守的微生物蛋白,即热休克蛋白(hsps),可用于有效预防和治疗关节炎。这种保护作用是通过诱导对自身hsps的交叉反应性T细胞应答来介导的。在JIA中,对hsps的天然T细胞免疫应答与少关节型JIA的疾病缓解相关。此外,这些应答与具有调节表型的T细胞的诱导有关。综上所述,这些数据表明,用hsps进行免疫调节可能是恢复天然T细胞应答从而治疗JIA和类风湿性关节炎的有效方法。

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本文引用的文献

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Inhibition of adjuvant-induced arthritis by interleukin-10-driven regulatory cells induced via nasal administration of a peptide analog of an arthritis-related heat-shock protein 60 T cell epitope.通过经鼻给予关节炎相关热休克蛋白60 T细胞表位的肽类似物诱导的白细胞介素-10驱动的调节性细胞对佐剂诱导的关节炎的抑制作用。
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Induction of IL-10 and inhibition of experimental arthritis are specific features of microbial heat shock proteins that are absent for other evolutionarily conserved immunodominant proteins.诱导白细胞介素-10及抑制实验性关节炎是微生物热休克蛋白的特异性特征,而其他进化上保守的免疫显性蛋白则不具备这些特征。
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Autoimmunity provoked by infection: how good is the case for T cell epitope mimicry?感染引发的自身免疫:T细胞表位模拟的证据有多充分?
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Chemokine receptor CCR4 on CD4+ T cells in juvenile rheumatoid arthritis synovial fluid defines a subset of cells with increased IL-4:IFN-gamma mRNA ratios.幼年类风湿性关节炎滑液中CD4+ T细胞上的趋化因子受体CCR4定义了一组白细胞介素-4与γ干扰素信使核糖核酸比例升高的细胞亚群。
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