The methylation levels of IFNG -54 CpG and -4293 CpG were negatively correlated with the age in HD, especially severe HD, patients and GD patients, respectively.
Treatment with EGCG significantly reduced interleukin-1β, interferon-γ (INF-γ) and tumor necrosis factor-α (TNF-α) levels in the AIT rats through suppression of nuclear factor-κB (NF-κB) pathway.
Taken together, these results suggest that lack of Cav-1 expression inhibited autophagy activity in TFC exposed to Th1 cytokines (IL-1β and IFN-γ), which might be a novel pathogenetic mechanism of HT.
Furthermore, strong positive correlations between the increased transcript level of IFNG-AS1 and the increased transcript level of T-bet or IFNG were revealed in thyroid tissues from HT patients.
Our results showed that the expression levels of Th1 cells-related T-bet and interferon-gamma (IFN-gamma) mRNA in PBMC from HT significantly decreased.
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-γ on IL-18 expression in isolated human thyroid follicular cells (TFCs).
Therefore, the present study, together with a previous report demonstrating the importance of Th1, not Th2, immune response for developing thyroiditis using mice deficient for interferon-gamma or IL-4, clearly indicates that both Th1 and Th17 cells are critical T(eff) subsets for the pathogenesis of spontaneous autoimmune thyroiditis in nonobese diabetic-H2(h4) mice.
The high IFN-gamma-producing allele T was observed to be associated with Hashimoto's thyroiditis in the present study where as in Graves' hyperthyroidism the association was observed to be stronger with the low producing allele A.
To conclude the results of the study suggest a differential association of high- and low-producing alleles of IFN-gamma gene with Hashimoto's thyroiditis and Graves' disease.
Interferon gamma promoted caspase up-regulation and CD95-induced apoptosis in HT thyrocytes, whereas interleukin 4 and interleukin 10 protected GD thyrocytes by potent up-regulation of cFLIP and Bcl-xL, which prevented CD95-induced apoptosis in sensitized thyrocytes.