Suppr超能文献

利用疾病生物学来理解和指导 JIA 的治疗。

Using biology of disease to understand and guide therapy of JIA.

机构信息

Department of Pediatric Immunology/Rheumatology, University Medical Centre Utrecht, Wilhelmina Children's Hospital, Lundlaan 6/Postbus 85090, 3584 EA/3508 AB Utrecht, The Netherlands.

出版信息

Best Pract Res Clin Rheumatol. 2009 Oct;23(5):599-608. doi: 10.1016/j.berh.2009.07.003.

Abstract

Juvenile idiopathic arthritis (JIA) is a heterogeneous, multi-factorial disease. The ability to distinguish various subtypes of JIA has enabled more directed and uniform clinical care. Possible triggers of the disease include genetic and environmental factors such as infections and vaccinations. Autoreactive T cells responding to unknown antigens are among the mechanisms that perpetuate the cycle of autoimmune inflammation once established. There are two groups of candidate auto-antigens that are thought to play a role in induction or modulation of T-cell responses. The first group is derived from cartilage and other joint-related tissue and the second group is derived from stress proteins. Several molecules have been implicated in the quest to restore immune homeostasis and tolerance, such as regulatory T cells, FoxP3, heat shock proteins, cytokines, chemokines and other key mediators of inflammation. Treatment strategies might focus on the induction of regulation in a more specific fashion.

摘要

幼年特发性关节炎(JIA)是一种异质性、多因素疾病。能够区分 JIA 的各种亚型使得能够进行更有针对性和更统一的临床护理。疾病的可能诱因包括遗传和环境因素,如感染和疫苗接种。一旦自身免疫炎症建立,针对未知抗原的自身反应性 T 细胞就是使该循环持续存在的机制之一。有两组候选自身抗原被认为在诱导或调节 T 细胞反应中发挥作用。第一组来自软骨和其他关节相关组织,第二组来自应激蛋白。在寻求恢复免疫稳态和耐受的过程中,有几个分子被牵涉其中,如调节性 T 细胞、FoxP3、热休克蛋白、细胞因子、趋化因子和其他炎症关键介质。治疗策略可能侧重于更有针对性地诱导调节。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验