TY - JOUR
T1 - Prevention of lymphocytic thyroiditis in iodide-treated non-obese diabetic mice lacking interferon regulatory factor-1
AU - Tani, Jun Ichi
AU - Mori, Kouki
AU - Hoshikawa, Saeko
AU - Nakazawa, Tetsuya
AU - Satoh, Jo
AU - Nakagawa, Yoshinori
AU - Ito, Sadayoshi
AU - Yoshida, Katsumi
PY - 2002/12/1
Y1 - 2002/12/1
N2 - 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.
AB - 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.
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U2 - 10.1530/eje.0.1470809
DO - 10.1530/eje.0.1470809
M3 - Article
C2 - 12457457
AN - SCOPUS:0036920263
VL - 147
SP - 809
EP - 814
JO - European Journal of Endocrinology
JF - European Journal of Endocrinology
SN - 0804-4643
IS - 6
ER -
