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• W1580102746 abstract "The process of inflammation, the disease itself, and the genetic background may all influence the response of patients to glucocorticoids (GCs). GC-dependent patients respond normally to GC but relapse once GCs are withdrawn or at dose tapering. A GC-resistant patient does not respond to GCs. The clinical response to GC can be correlated with in vitro leukocyte sensitivity to glucocorticoids. GC resistance in inflammatory diseases is not genetically determined. Cytokines, such as interleukin (IL)-1β, IL-6, tumor necrosis factor alpha (TNF-α), interferon-γ (IFNγ), IL-2, IL-4, and IL-13, modulate glucocorticoid receptor (GR) numbers and binding affinity with parallel changes of GC sensitivity. Certain cytokine-stimulated transcription factors may interact in the nucleus with ligand-activated GRα and prevent ligand-activated GRα either from binding to glucocorticoid-responsive elements (GREs) or from exerting its transcriptional actions. Cytokines may directly target the GR through post-translational mechanisms. Phosphorylation and dephosphorylation of the receptor may participate in the ligand activation/inactivation, recycling, and turnover of the receptor. Excessive nuclear factor (NF)-κB, activator protein-1 (AP-1), signal transducers and activators of transcription (STAT) expression, and activity in an inflammatory site might inhibit GC activity, contributing to a decrease in GC sensitivity. The combinatorial interactions of co-activators and co-repressors with the nuclear receptors may explain the cell and tissue selectivity of nuclear receptor actions. Such co-regulators could undergo post-translational modifications and integrate multiple signals from different signaling pathways such as the mitogen-activated protein kinase (MAPK) pathway. The expression of 11β-hydroxysteroid dehydrogenase, which regulates intracellular active GC metabolite concentration, may be modulated by cytokines, enhancing or decreasing GC sensitivity. The multi-drug resistance-1 (MDR-1) gene product P-glycoprotein 170 is a membrane-based drug-efflux pump, which transports GCs out of the cells, thereby lowering intracellular active GC concentration. Finally, alterations of post-receptor mechanisms in the GC-signaling pathway and transcription machinery may account for resistance in some patients with familial GC resistance." @default.
• W1580102746 created "2016-06-24" @default.
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• W1580102746 date "2007-01-01" @default.
• W1580102746 modified "2023-09-25" @default.
• W1580102746 title "Glucocorticoid Resistance in Inflammatory Diseases" @default.
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• W1580102746 doi "https://doi.org/10.1016/s1567-7443(07)00218-9" @default.
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