Todd I, Pujol-Borrell R, Hammond L J, McNally J M, Feldmann M, Bottazzo G F
Department of Immunology, Middlesex Hospital Medical School, London, UK.
Clin Exp Immunol. 1987 Sep;69(3):524-31.
HLA Class II molecules are expressed by human thyroid epithelial cells (thyrocytes) in thyroid autoimmunity, although these cells are normally Class II-. gamma-Interferon (gamma-IFN) is probably involved in this expression, as suggested by its ability to induce Class II in cultured normal thyrocytes. We have now found that thyroid stimulating hormone (TSH) enhances Class II expression induced in cultured thyrocytes by gamma-IFN, and effects similar to those of TSH were obtained with dibutyryl cyclic AMP. A proportion of thyrocytes also expressed Class II following treatment with TSH or dibutyryl cyclic AMP in the absence of gamma-IFN, but the optimal activity of these mediators then appeared to be dependent upon the occurrence of some pre-existing Class II expression. These findings give insights into how a variety of mediators may influence Class II expression in thyroid autoimmunity.
在甲状腺自身免疫中,人类甲状腺上皮细胞(甲状腺细胞)可表达HLA - II类分子,尽管这些细胞通常不表达II类分子。γ - 干扰素(γ - IFN)可能参与了这种表达,这是由其在培养的正常甲状腺细胞中诱导II类分子表达的能力所表明的。我们现在发现,促甲状腺激素(TSH)可增强γ - IFN在培养的甲状腺细胞中诱导的II类分子表达,并且用二丁酰环磷腺苷(dibutyryl cyclic AMP)可获得与TSH相似的效果。在没有γ - IFN的情况下,一部分甲状腺细胞在用TSH或二丁酰环磷腺苷处理后也表达了II类分子,但这些介质的最佳活性似乎取决于一些预先存在的II类分子表达的发生情况。这些发现为多种介质如何影响甲状腺自身免疫中的II类分子表达提供了见解。