• arthritis
• experimental
• glucocorticoids
• inflammation

Glucocorticoids are highly effective drugs that are used very widely to inhibit inflammation and to modulate the immune system.1–3 Their great importance in the treatment of various rheumatic diseases is undisputed.4–7 However, although their introduction into clinical medicine was more than 70 years ago, we have understood only a fraction of their mechanisms of action. This is mainly due to their highly pleiotropic effects.8 9 A therapeutically used monoclonal antibody against tumour necrosis factor alpha (TNFalpha) neutralises this molecule, and that is it. In contrast, glucocorticoids as hormones regulate an estimated 20% of the entire genome.10 11 The synthesis of cytokines, chemokines, adhesion molecules, receptors and many enzymes, mediators and other proteins is either upregulated or downregulated. In addition, various mechanisms of their action exist whereby we distinguish between genomic and non-genomic effects. These underlying mechanisms of action are known in principle and discussed in detail elsewhere,3 12–14 so the current knowledge is only summarised here in the form of table 1. However, our understanding of glucocorticoid-mediated immunoregulation still has substantial gaps, not only but especially regarding effects of glucocorticoids in specific cell types and their key cellular targets in particular disease states, and the actions these hormones broadly induce in cells and tissues versus those that are unique to the immune system.9 15