Mori Kouki, Yoshida Katsumi, Mihara Masahiko, Ohsugi Yoshiyuki, Nakagawa Yoshinori, Hoshikawa Saeko, Ozaki Hiroshi, Ito Sadayoshi
Tohoku University Graduate School of Medicine, Sendai, Japan.
Autoimmunity. 2009 Mar;42(3):228-34. doi: 10.1080/08916930802709141.
We explored the role of interleukin-6 (IL-6) in the development of autoimmune thyroiditis in nonobese diabetic (NOD) mice, an animal model of Hashimoto's thyroiditis, using anti-mouse IL-6 receptor antibody (MR16-1). Thyroiditis was induced by iodide ingestion or mouse thyroglobulin (Tg) immunization. Mice were injected intraperitoneally with saline, control rat IgG, or MR16-1 (2 or 8 mg). Iodide ingestion did not increase serum IL-6 levels and MR16-1 (2 mg) failed to prevent the development of thyroiditis. In contrast, Tg immunization induced a rapid and significant increase in serum IL-6 levels. While MR16-1 (2 mg) had no effect on Tg-induced thyroiditis, the severity, but not incidence, of thyroiditis was reduced in 8 mg MR16-1-treated mice compared with saline-injected mice. However, thyroiditis development in the 8 mg MR16-1-treated mice was indistinguishable from that in the control IgG-treated mice. MR16-1 (8 mg) did not affect serum anti-Tg antibody levels. These results suggest that IL-6 may play only a minor role in the development of autoimmune thyroiditis in NOD mice.
我们使用抗小鼠白细胞介素-6受体抗体（MR16-1），在桥本甲状腺炎的动物模型——非肥胖糖尿病（NOD）小鼠中，探究了白细胞介素-6（IL-6）在自身免疫性甲状腺炎发展过程中的作用。通过摄入碘化物或免疫小鼠甲状腺球蛋白（Tg）诱导甲状腺炎。给小鼠腹腔注射生理盐水、对照大鼠IgG或MR16-1（2毫克或8毫克）。摄入碘化物并未增加血清IL-6水平，且MR16-1（2毫克）未能预防甲状腺炎的发展。相比之下，免疫Tg可导致血清IL-6水平迅速且显著升高。虽然MR16-1（2毫克）对Tg诱导的甲状腺炎没有影响，但与注射生理盐水的小鼠相比，接受8毫克MR16-1治疗的小鼠甲状腺炎的严重程度降低，但发病率未降低。然而，接受8毫克MR16-1治疗的小鼠甲状腺炎的发展与接受对照IgG治疗的小鼠并无差异。MR16-1（8毫克）不影响血清抗Tg抗体水平。这些结果表明，IL-6在NOD小鼠自身免疫性甲状腺炎的发展过程中可能仅起次要作用。
