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Division of Nephrology, Endocrinology and Vascular Medicine and
¹ Division of Rheumatology and Hematology, Tohoku University Graduate School of Medicine, 1-1 Seiryo-machi, Aoba-ku, Sendai 980-8574, Japan

(Requests for offprints should be addressed to K Mori; Email: kokimori{at}mail.tains.tohoku.ac.jp)

Tumor necrosis factor- (TNF) may play a role in the development of autoimmune thyroiditis such as Hashimoto’s thyroiditis. In the present study, we examined whether TNF induced its own expression in FRTL-5 rat thyroid cells. Lipopolysaccharide (LPS) markedly increased TNF mRNA levels in FRTL-5 cells as assessed by semiquantitative RT-PCR. In addition, LPS-stimulated cells released TNF protein into the culture medium. Similarly, TNF induced its own gene and protein expression in FRTL-5 cells as assessed by RT-PCR and metabolic labeling and immunoprecipitation of TNF. The autoinduction of TNF gene was also observed in TNF-stimulated human thyroid epithelial cells. TNF induction was specific to LPS and TNF since interferon- or amiodarone failed to increase TNF mRNA levels in FRTL-5 cells. Human TNF induced rat TNF gene expression, indicating that type 1 TNF receptor (TNF-R) is involved in the autoinduction. TNF 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 TNF. Although the biological significance of autoinduction of TNF remains unclear, our results suggest that thyroid epithelial cells may participate in the development of autoimmune thyroiditis through production of TNF. Furthermore, inhibition of TNF production in the thyroid may represent a novel approach to mitigating inflammation in autoimmune thyroiditis.