Autoinduction of tumor necrosis factor- in FRTL-5 rat thyroid cells

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, LPSstimulated 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 interferonor 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. Journal of Endocrinology (2005) 187, 17–24