Kang Bong-Seok, Chung Tae-Wook, Moon Jin-Young, Lim Jong-Kook, Shon Yun-Hee, Nam Kyung-Soo, Kim Dong-Soo, Jeon Byung-Hoon, Kim Cheorl-Ho
Department of Biochemistry, Molecular Biology and AM-Pointology, Dongguk University College of Oriental Medicine and National Research Laboratory for Glycobiology, Kyungju, Kyungbuk, South Korea.
Immunopharmacol Immunotoxicol. 2004 Aug;26(3):355-72. doi: 10.1081/iph-200026872.
Contribution of cytotoxic T lymphocytes (CTL) to experimental autoimmune thyroiditis (EAT) was well defined (Speidel et al., Eur. J. Immunol. 1997, 27, 2391-2399, Ref. 7). The native porcine thyroglobulin (pTg) showed high sensitivity to endo-o-N-acetylglucosaminidase F (Endo F) and its molecular weights, corresponding to about 330 kDa as a monomer and 660 kDa as a dimer, were reduced to smaller molecular weight forms by Endo F and trifluoromethanesulfonic acid (TMSF). Deglycosylated porcine Tg (dgpTg) and native pTg were injected i.v. into CBA/J mice, without the aid of adjuvants. Both lymphocytic infiltrations of the thyroid glands and levels of Tg-specific CTL were similar to those found in conventional EAT induced by Tg and adjuvants. In contrast, proliferative responses in native pTg and dgpTg-injected mice could not be detected, and titers of antibodies to pTg and dgpTg were 20 times and 30 times lower than that of pTg and adjuvants, respectively. The EAT-inducer CTL belonged to the CD8+ cell subset and exerted their thyroiditogenic potential through release of IFN-gamma. It was concluded that dgpTg-induced EAT is mediated by type 1 cytotoxic T cells (Tcl). Also, results that EAT induction of the glycosylated pTg (gpTg) was much lower than that of dgpTg, suggested that the abberant and incomplete glycosylation of the thyroglobulin is responsible for the induction of autoimmune thyroiditis.
细胞毒性T淋巴细胞（CTL）在实验性自身免疫性甲状腺炎（EAT）中的作用已得到明确界定（Speidel等人，《欧洲免疫学杂志》，1997年，27卷，2391 - 2399页，参考文献7）。天然猪甲状腺球蛋白（pTg）对内切 - o - N - 乙酰葡糖胺酶F（Endo F）表现出高敏感性，其分子量，单体约为330 kDa，二聚体约为660 kDa，经Endo F和三氟甲磺酸（TMSF）处理后降低为较小分子量形式。去糖基化猪Tg（dgpTg）和天然pTg经静脉注射到CBA/J小鼠体内，无需佐剂。甲状腺的淋巴细胞浸润和Tg特异性CTL水平与由Tg和佐剂诱导的传统EAT中发现的情况相似。相比之下，在注射天然pTg和dgpTg的小鼠中未检测到增殖反应，并且针对pTg和dgpTg的抗体滴度分别比pTg和佐剂诱导的情况低20倍和30倍。诱导EAT的CTL属于CD8 +细胞亚群，并通过释放γ干扰素发挥其致甲状腺炎潜能。得出的结论是，dgpTg诱导的EAT由1型细胞毒性T细胞（Tcl）介导。此外，糖基化pTg（gpTg）诱导EAT的能力远低于dgpTg的结果表明，甲状腺球蛋白异常和不完全的糖基化是自身免疫性甲状腺炎诱导的原因。
