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Kouki Mori, Katsumi Yoshida, Ayumi Komatsu, Jun-ichi Tani, Yoshinori Nakagawa, Saeko Hoshikawa and Sadayoshi Ito

Tumor necrosis factor-α (TNFα) may play a role in the development of autoimmune thyroiditis such as Hashimoto’s thyroiditis. In the present study, we examined whether TNFα induced its own expression in FRTL-5 rat thyroid cells. Lipopolysaccharide (LPS) markedly increased TNFα mRNA levels in FRTL-5 cells as assessed by semiquantitative RT-PCR. In addition, LPS-stimulated cells released TNFα protein into the culture medium. Similarly, TNFα induced its own gene and protein expression in FRTL-5 cells as assessed by RT-PCR and metabolic labeling and immunoprecipitation of TNFα. The autoinduction of TNFα gene was also observed in TNFα-stimulated human thyroid epithelial cells. TNFα induction was specific to LPS and TNFα since interferon-α or amiodarone failed to increase TNFα mRNA levels in FRTL-5 cells. Human TNFα induced rat TNFα gene expression, indicating that type 1 TNF receptor (TNF-R) is involved in the autoinduction. TNFα did not increase either type 1 or type 2 TNF-R mRNA levels, suggesting that upregulation of TNF receptors is not involved in the autoinduction of TNFα. Although the biological significance of autoinduction of TNFα remains unclear, our results suggest that thyroid epithelial cells may participate in the development of autoimmune thyroiditis through production of TNFα. Furthermore, inhibition of TNFα production in the thyroid may represent a novel approach to mitigating inflammation in autoimmune thyroiditis.