Nature's choice of genes controlling chronic inflammation.

R Holmdahl
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引用次数: 2

Abstract

Inflammation is a physiological response that may go uncontrolled and thereby develop in a chronic way. This seems to happen in many common diseases of autoimmune, degenerative, or allergic character. Rheumatoid arthritis (RA) is by definition a chronic disease with an autoimmune inflammatory attack on diarthrodial cartilaginous joints. The development of new treatment neutralizing cytokines involved in the inflammatory attack has given relief and gives the promise of more effective treatment of already established disease. It is now time to set our eyes on a new vision to develop preventive and curative treatment based on knowledge of the unique and causative pathogenic mechanisms. To do this we believe it is important to identify the natural-selected polymorphisms that are associated with disease. These have proven to be extremely difficult to identify in complex diseases such as RA, but using animal models, this work is closer to reality. Animal models have recently been developed mimicking various aspects of the human disease. We will present an example in which a genetic polymorphism associated with the development of arthritis has been identified. On the basis of this finding, a new pathway involving control of immune tolerance by reactive oxidative species has been identified and a new class of antiinflammatory agents activating the induced oxidative burst protein complex is suggested.

自然选择控制慢性炎症的基因。
炎症是一种生理反应,可能无法控制,从而以慢性方式发展。这似乎发生在许多自身免疫性疾病、退行性疾病或过敏性疾病中。类风湿关节炎(RA)的定义是一种慢性疾病与自身免疫性炎症发作的软骨关节。新疗法的发展中和了参与炎症攻击的细胞因子,缓解了病情,并为更有效地治疗已经建立的疾病提供了希望。现在,我们应该着眼于一个新的愿景,即在了解独特的致病机制的基础上发展预防性和治疗性治疗。要做到这一点,我们认为确定与疾病相关的自然选择多态性是很重要的。这些已被证明在诸如类风湿性关节炎等复杂疾病中极难识别,但使用动物模型,这项工作更接近现实。最近已经开发出动物模型来模仿人类疾病的各个方面。我们将提出一个例子,其中遗传多态性与关节炎的发展已被确定。在此基础上,研究人员发现了一条通过氧化反应调控免疫耐受的新途径,并提出了一类激活氧化爆发蛋白复合物的新型抗炎药。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
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