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白细胞介素-6阻断对非肥胖糖尿病小鼠自身免疫性甲状腺炎发展的影响。

Effects of interleukin-6 blockade on the development of autoimmune thyroiditis in nonobese diabetic mice.

作者信息

Mori Kouki, Yoshida Katsumi, Mihara Masahiko, Ohsugi Yoshiyuki, Nakagawa Yoshinori, Hoshikawa Saeko, Ozaki Hiroshi, Ito Sadayoshi

机构信息

Tohoku University Graduate School of Medicine, Sendai, Japan.

出版信息

Autoimmunity. 2009 Mar;42(3):228-34. doi: 10.1080/08916930802709141.

Abstract

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.

摘要

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。

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