Li H S, Verginis P, Carayanniotis G
Division of Endocrinology, Faculty of Medicine, Memorial University of Newfoundland, St. John's, NL, Canada.
Clin Exp Immunol. 2006 Jun;144(3):467-74. doi: 10.1111/j.1365-2249.2006.03080.x.
Dendritic cell (DC) maturation is required for efficient presentation of autoantigens leading to autoimmunity. In this report, we have examined whether release of tissue antigens from necrotic thyroid epithelial cells can trigger DC maturation and initiation of a primary anti-self response. DC were cocultured with either viable (VT/DC) or necrotic (NT/DC) thyrocytes, and their phenotypic and functional maturation as well as immunopathogenic potential were assessed. Significant up-regulation of surface MHC class II and costimulatory molecule expression was observed in NT/DC but not in VT/DC. This was correlated with a functional maturation of NT/DC, determined by IL-12 secretion. Challenge of CBA/J mice with NT/DC, but not with VT/DC, elicited thyroglobulin (Tg)-specific IgG as well as Tg-specific CD4(+) T-cell responses and led to development of experimental autoimmune thyroiditis. These results support the view that thyroid epithelial cell necrosis may cause autoimmune thyroiditis via maturation of intrathyroidal DC.
树突状细胞(DC)成熟是自身抗原有效呈递导致自身免疫所必需的。在本报告中,我们研究了坏死甲状腺上皮细胞释放的组织抗原是否能触发DC成熟并引发初次抗自身反应。将DC与活的(VT/DC)或坏死的(NT/DC)甲状腺细胞共培养,并评估其表型和功能成熟以及免疫致病潜力。在NT/DC中观察到表面MHC II类分子和共刺激分子表达显著上调,而在VT/DC中未观察到。这与由IL-12分泌所确定的NT/DC功能成熟相关。用NT/DC而非VT/DC攻击CBA/J小鼠,引发了甲状腺球蛋白(Tg)特异性IgG以及Tg特异性CD4(+) T细胞反应,并导致实验性自身免疫性甲状腺炎的发生。这些结果支持这样一种观点,即甲状腺上皮细胞坏死可能通过甲状腺内DC的成熟导致自身免疫性甲状腺炎。