Glucocorticoid modulation of human monocyte/macrophage function: Control of TNF-α secretion
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Glucocorticoids suppress many functions in activated monocyte/macrophages, including the release of TNF-α. This is likely to contribute to the efficacy of glucocorticoids in some inflammatory diseases, such as rheumatoid arthritis, where TNF-α contributes to pathogenesis. Glucocorticoids suppress the activity of reporters which include TNF-α promoter regions and modify the activity of NF-κB family transcription factors in activated human monocytic cell lines, suggesting effects of glucocorticoids on TNF-α gene transcription. In addition, glucocorticoids have been reported to antagonise the enhanced translational efficiency of TNF-α mRNA which occurs at least after stimulation of murine monocytic cells. It is likely, therefore, that glucocorticoids act at several points in stimulated monocyte/macrophages to reduce TNF-α secretion. Understanding glucocorticoid control of TNF-α secretion may explain some of the variability in response to GC in inflammatory diseases and may reveal means of inducing glucocorticoid-like anti-inflammatory effects in monocyte/macrophages without exposing other tissues to the adverse effects of glucocorticoids.
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