Glucocorticoids are among the most widely used agents for the treatment of inflammatory diseases. The primary mechanism of glucocorticoid action is via the glucocorticoid receptor (GR), which blocks the expression of proinflammatory cytokines and adhesion molecules. Repression of many pro-inflammatory genes occurs by inhibition of transcription factors including nuclear factor kappaB (NFkappaB) and activator protein-1 (AP-1). In this article, we discuss the physiological and molecular interaction that occurs between GR and proinflammatory cytokines signaling pathways.
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Hermoso et al. (2003) studied this question.
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