Prevention of lymphocytic thyroiditis in iodide-treated non-obese diabetic mice lacking interferon regulatory factor-1

Jun Ichi Tani, Kouki Mori, Saeko Hoshikawa, Tetsuya Nakazawa, Jo Satoh, Yoshinori Nakagawa, Sadayoshi Ito, Katsumi Yoshida

研究成果: Article査読

18 被引用数 (Scopus)

抄録

Objective: Interferon regulatory factor-1 (IRF-1) is a critical regulator of interferon-γ (IFNγy)-mediated immune responses. To determine whether IRF-1 is involved in the pathogenesis of thyroiditis in animal models, we evaluated the incidence of iodide-induced lymphocytic thyroiditis (LT) in non-obese diabetic (NOD) mice lacking IRF-1 as well as IRF-1 +/+ and +/- mice. Design: IRF-1 +/+, +/- and -/- NOD mice at 6 weeks of age were fed water (group 1) or iodide water (group 2) for 8 weeks. Methods: Thyroids were examined histopathologically and intrathyroidal lymphocytic infiltration was arbitrarily graded. Serum thyroxine (T4) and anti-mouse thyroglobulin antibody (anti-mTgAb) levels were measured. Spleen cell population was analyzed by flow cytometry, and IFNγ and interleukin-10 produced by splenocytes were measured by enzyme-linked immunosorbent assay. Results: In group 1, only 4.3% of NOD mice developed LT. In contrast, 67.6% of mice in group 2 developed the disease. Iodide treatment induced LT in more than 80% of IRF-1 +/+ and +/- mice. However, no IRF-1 -/- mice in group 2 developed LT. There was no difference in both serum anti-mTgAb and T4 levels among the three IRF-1 genotypes of NOD mice. Numbers of splenic CD8+ T cells and IFN-γ production by Concanavalin A-stimulated splenocytes were markedly decreased in IRF-1-deficient NOD mice. Conclusions: IRF-1 is involved in the development of iodide-induced LT in NOD mice.

本文言語English
ページ(範囲)809-814
ページ数6
ジャーナルEuropean Journal of Endocrinology
147
6
DOI
出版ステータスPublished - 2002 12月 1
外部発表はい

ASJC Scopus subject areas

  • 内分泌学、糖尿病および代謝内科学
  • 内分泌学

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