[Role of apoptosis in autoimmune thyroid disorders].

Artur Bossowski, Anna Moniuszko, Joanna Bouzyk, Mirosława Urban
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Abstract

Apoptosis, programmed cell death, is a physiological phenomenon, necessary for normal function of every organism. This is an active process, per-current with a participation of the cellular metabolism embracing the activation of genes and the synthesis of proteins. The signal to apoptosis can be started practically in every cell of our organism. Disturbances of the apoptosis regulation determine the essential link of the pathogenesis of many diseases, including autoimmune thyroid disorders. Such molecules as FasL, TNF (tumor necrosis factor), TRAIL (the ligand inducing apoptosis), inducing different apoptotic pathway can play the key-role in the pathogenesis of Graves' disease or Hashimoto's thyroiditis. Besides in the destructive thyroiditis an important role is also played by proteins from the bcl-2 family and the proinflammatory cytokines. The aim of this publication is to present the influence of different factors on the apoptosis and the role of programmed cells death in autoimmune thyroid diseases.

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凋亡在自身免疫性甲状腺疾病中的作用
细胞凋亡,即细胞程序性死亡,是一种生理现象,是机体正常功能所必需的。这是一个活跃的过程,目前参与了细胞代谢,包括基因的激活和蛋白质的合成。凋亡的信号几乎可以在我们生物体的每一个细胞中开始。细胞凋亡调控的紊乱决定了包括自身免疫性甲状腺疾病在内的许多疾病发病机制的重要环节。FasL、TNF(肿瘤坏死因子)、TRAIL(诱导凋亡的配体)等分子,诱导不同的凋亡通路,在Graves病或桥本甲状腺炎的发病机制中发挥关键作用。此外,在破坏性甲状腺炎中,bcl-2家族蛋白和促炎细胞因子也起着重要作用。本文的目的是介绍不同因素对自身免疫性甲状腺疾病中细胞凋亡的影响和程序性细胞死亡的作用。
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