PMID- 20586818 OWN - NLM STAT- MEDLINE DCOM- 20101217 LR - 20211020 IS - 1365-2613 (Electronic) IS - 0959-9673 (Print) IS - 0959-9673 (Linking) VI - 91 IP - 5 DP - 2010 Oct TI - Thyrocyte interleukin-18 expression is up-regulated by interferon-gamma and may contribute to thyroid destruction in Hashimoto's thyroiditis. PG - 420-5 LID - 10.1111/j.1365-2613.2010.00715.x [doi] AB - Interferon-gamma (IFN-gamma) has a direct role in thyroid destruction in autoimmune thyroiditis. Interleukin-18 (IL-18), a pro-inflammatory cytokine with potent IFN-gamma inducing activities, may play an important role in Th1-mediated autoimmune diseases. The purpose of this study was to characterize the expression and localization of IL-18 in the thyroid tissues of Hashimoto's thyroiditis (HT) and to investigate the effect of IFN-gamma on IL-18 expression in isolated human thyroid follicular cells (TFCs). Thyroid tissues obtained from six euthyroid patients with HT and six control subjects were used to detect IL-18 expression by reverse transcription-polymerase chain reaction (RT-PCR) and immunohistochemical staining. Human TFCs were isolated and incubated for 48 h with or without IFN-gamma, tumour necrosis factor-alpha (TNF-alpha) or IL-1beta. IL-18 expression was analysed by RT-PCR, immunofluorescent double staining and western blot. We found that IL-18 expression was increased in the thyroid tissues of HT compared with control thyroid tissues. TFCs were major cell types expressing IL-18 in the thyroid tissues of HT. IL-18 was constitutively expressed in isolated human TFCs, and the expression was significantly up-regulated by IFN-gamma rather than TNF-alpha or IL-1beta. Western bolt revealed that a 24-kDa band corresponding to pro-IL-18 was broadened in the lysates of IFN-gamma-treated TFCs. Our results demonstrated that IL-18 expression is up-regulated in the TFCs of HT patients and in primary human TFCs exposed to IFN-gamma. Therefore, intrathyroidal interaction between IL-18 and IFN-gamma may have a role in promoting the local immune response, which contributes to the thyroid destruction seen in HT. CI - (c) 2010 The Authors. Journal compilation (c) 2010 Blackwell Publishing Ltd. FAU - Liu, Zhe AU - Liu Z AD - Department of Endocrinology and Metabolism, Peking University Third Hospital, Beijing, China. FAU - Wang, Haining AU - Wang H FAU - Xiao, Wenhua AU - Xiao W FAU - Wang, Chen AU - Wang C FAU - Liu, Guoqiang AU - Liu G FAU - Hong, Tianpei AU - Hong T LA - eng PT - Journal Article PT - Research Support, Non-U.S. Gov't PL - England TA - Int J Exp Pathol JT - International journal of experimental pathology JID - 9014042 RN - 0 (Interleukin-18) RN - 0 (Interleukin-1beta) RN - 0 (Tumor Necrosis Factor-alpha) RN - 82115-62-6 (Interferon-gamma) SB - IM MH - Adult MH - Biopsy MH - Cells, Cultured MH - Female MH - Gene Expression/immunology MH - Hashimoto Disease/immunology/metabolism/*pathology MH - Humans MH - Interferon-gamma/*metabolism MH - Interleukin-18/*genetics/*metabolism MH - Interleukin-1beta/metabolism MH - Male MH - Middle Aged MH - Thyroid Gland/immunology/metabolism/*pathology MH - Tumor Necrosis Factor-alpha/metabolism MH - Up-Regulation/immunology PMC - PMC3003839 EDAT- 2010/07/01 06:00 MHDA- 2010/12/18 06:00 PMCR- 2011/10/01 CRDT- 2010/07/01 06:00 PHST- 2010/07/01 06:00 [entrez] PHST- 2010/07/01 06:00 [pubmed] PHST- 2010/12/18 06:00 [medline] PHST- 2011/10/01 00:00 [pmc-release] AID - IEP715 [pii] AID - 10.1111/j.1365-2613.2010.00715.x [doi] PST - ppublish SO - Int J Exp Pathol. 2010 Oct;91(5):420-5. doi: 10.1111/j.1365-2613.2010.00715.x.