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目的 本文研究白介素１（ Ｉ Ｌ１） 、干扰素α（ Ｉ Ｆ Ｎα） 和肿瘤坏死因子（ Ｔ Ｎ Ｆ） 对人正常甲状腺细胞环磷酸腺苷（ｃ Ａ Ｍ Ｐ） 生成的影响。方法 运用人甲状腺细胞原代培养技术和放免分析技术，检测不同种类细胞因子刺激甲状腺细胞引起的ｃ Ａ Ｍ Ｐ 释放状况。结果 （１） Ｉ Ｌ１ 、 Ｉ Ｆ Ｎα和 Ｔ Ｎ Ｆ 均可促进甲状腺细胞基础ｃ Ａ Ｍ Ｐ 的释放。（２） Ｉ Ｌ１ 在１０ － ３ ～１０３ Ｕ／ｍｌ 的浓度范围内，可明显增强促甲状腺激素（ Ｔ Ｓ Ｈ） 对甲状腺细胞生成ｃ Ａ Ｍ Ｐ 的刺激效应，其中以１０ － １ Ｕ／ｍｌ 的 Ｉ Ｌ１ 作用最强。（３） Ｉ Ｆ Ｎα对 Ｔ Ｓ Ｈ 刺激甲状腺细胞ｃ Ａ Ｍ Ｐ 的生成具有双向调节作用，１０ － ２ ～１ Ｕ／ ｍｌ 可增加ｃ Ａ Ｍ Ｐ 释放，而１０３ Ｕ／ｍｌ 时则抑制 Ｔ Ｓ Ｈ 的刺激效应。（４）１０ ～１０４ Ｕ／ｍｌ 的 Ｔ Ｎ Ｆ 使 Ｔ Ｓ Ｈ 刺激甲状腺细胞生成ｃ Ａ Ｍ Ｐ 的量显著减少。结论 多种细胞因子参与甲状腺功能的调节，并可能与自身免疫性甲状腺疾病的发生发展过程有一定关联。
Objective To investigate the effects of interleukin1 (IL1), interferon α (ILα) and tumor necrosis factor (TNF) on the production of cAMP in human normal thyroid cells influences. Methods Human primary cultured thyroid cells and radioimmunoassay (RIA) were used to detect the release of c A M P induced by different kinds of cytokines in thyrocytes. Results (1) I L 1, I F N α and T N F can promote thyroid cell basal cA M P release. (2) I L1 could significantly enhance the stimulatory effect of thyrotropin (T S H) on c A M P production by thyroid cells in the concentration range of 10 - 3 ~ 103 U / ml, of which 10 -1 U / Ml of the most effective I L 1. (3) I F Nαhad bidirectional modulation of THA-stimulated cA M P production in thyrocytes, 10 -2-1 U / ml increased c A M P release, while 103 U / ml inhibited T S H stimulation effect. (4) T N F at 10 ~ 104 U / ml significantly decreased the amount of c A M P that T S H stimulated thyroid cells to produce. Conclusion A variety of cytokines are involved in the regulation of thyroid function, and may be related to the occurrence and development of autoimmune thyroid disease.