Glucocorticoids exert anti-inflammatory and immunosuppressive activities by genomic and
nongenomic effects. The classic genomic effects are mediated by cytosolic glucocorticoid
receptors that can upregulate the expression of anti-inflammatory proteins in the nucleus
(transactivation) or repress the translocation of proinflammatory transcription factors from the
cytosol into the nucleus (transrepression). The nongenomic effects are probably mediated
by membrane glucocorticoid receptors. Glucocorticoid receptors are expressed also in …