Cytokines and thyroid function

R.A. Ajjan, P.F. Watson, A.P. Weetman
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引用次数: 96

Abstract

Cytokines play a crucial role in autoimmune thyroid disease (ATD) through various mechanisms. They are produced in the thyroid by intrathyroidal inflammatory cells, in particular lymphocytes, as well as by the thyroid follicular cells (TFC) themselves and may thus act in a cascade to enhance the autoimmune process (Fig.l). Cytokines upregulate the inflammatory reaction through stimulation of both T and B cells, resulting in antibody production and tissue injury. In addition, intrathyroidal cytokines induce immunological changes in TFC including enhancement of both major histocompatibility complex (MHC) class I and class II molecule expression, and upregulation of adhesion and complement regulatory molecule expression. Cytokines can also modulate both growth and function of TFC and have a role in extrathyroidal complications of ATD, most importantly thyroid-associated ophthalmopathy (TAO), where they induce fibroblast proliferation and enhance the production of glycosaminoglycans (GAG), resulting in proptosis and the other clinical features of the disease. In addition to these effects, exogenous administration of cytokines has been associated with impairment of thyroid function ranging from the appearance of autoantibodies

细胞因子与甲状腺功能
细胞因子通过多种机制在自身免疫性甲状腺疾病(ATD)中发挥重要作用。它们在甲状腺中由甲状腺内炎症细胞(特别是淋巴细胞)以及甲状腺滤泡细胞(TFC)本身产生,因此可能通过级联作用增强自身免疫过程(图1)。细胞因子通过刺激T细胞和B细胞上调炎症反应,导致抗体产生和组织损伤。此外,甲状腺内细胞因子诱导TFC的免疫学变化,包括主要组织相容性复合体(MHC) I类和II类分子表达的增强,以及粘附和补体调节分子表达的上调。细胞因子还可以调节TFC的生长和功能,并在ATD的甲状腺外并发症中发挥作用,最重要的是甲状腺相关性眼病(TAO),其中它们诱导成纤维细胞增殖并增强糖胺聚糖(GAG)的产生,导致纤维化和该疾病的其他临床特征。除了这些影响外,外源性给药细胞因子与甲状腺功能损害有关,包括自身抗体的出现
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