Braley-Mullen H, Tompson J G, Sharp G C, Kyriakos M
Cell Immunol. 1983 Feb 15;76(1):113-9. doi: 10.1016/0008-8749(83)90353-2.
Guinea pigs injected with guinea pig thyroglobulin (GPTG) in incomplete Freund's adjuvant (IFA) have been shown to be unresponsive to challenge with GPTG in complete Freund's adjuvant (CFA). However, effector cells which transfer experimental autoimmune thyroiditis (EAT) can be demonstrated in cultured lymph node cells (LNC) of unresponsive animals, indicating that GPTG in IFA does not suppress the initial sensitization of EAT effector cells. LNC from unresponsive animals were unable to suppress the in vitro activation of effector LNC or to suppress EAT when cotransferred with effector cells. When GPTG in IFA was given to animals which were used as recipients of effector cells, the production of EAT was markedly suppressed. These results suggest that GPTG in IFA can suppress EAT either by preventing effector cells from interacting with the thyroid or by interfering with the function of a cell in the normal recipient which may interact with effector cells to result in the lesions of EAT.
已证明，在不完全弗氏佐剂（IFA）中注射豚鼠甲状腺球蛋白（GPTG）的豚鼠，对在完全弗氏佐剂（CFA）中注射GPTG的攻击无反应。然而，在无反应动物的培养淋巴结细胞（LNC）中可证明能转移实验性自身免疫性甲状腺炎（EAT）的效应细胞，这表明IFA中的GPTG不会抑制EAT效应细胞的初始致敏。来自无反应动物的LNC在与效应细胞共转移时，无法抑制效应LNC的体外活化或抑制EAT。当将IFA中的GPTG给予用作效应细胞受体的动物时，EAT的产生会受到明显抑制。这些结果表明，IFA中的GPTG可以通过阻止效应细胞与甲状腺相互作用，或通过干扰正常受体中可能与效应细胞相互作用而导致EAT病变的细胞功能来抑制EAT。
