Glucocorticoids are potent anti-inflammatories, regardless of the inflammation's cause; their primary anti-inflammatory mechanism is lipocortin-1 (annexin-1) synthesis. Lipocortin-1 both suppresses phospholipase A2 , thereby blocking eicosanoid production, and inhibits various leukocyte inflammatory events ( epithelial adhesion , emigration , chemotaxis , phagocytosis , respiratory burst , etc.). In other words, glucocorticoids not only suppress immune response, but also inhibit the two main products of inflammation, prostaglandins and leukotrienes . They inhibit prostaglandin synthesis at the level of phospholipase A2 as well as at the level of cyclooxygenase /PGE isomerase (COX-1 and COX-2),  the latter effect being much like that of NSAIDs , potentiating the anti-inflammatory effect.
Stopping corticosteroid therapy
In autoimmune disease, clear end-points should be set before starting therapy. Corticosteroids may improve mood and give patients a feeling of general well-being unrelated to the effect on the disease being treated. Subjective assessments can therefore be misleading. Objective clinical parameters should be used to monitor the need for continuing or restarting therapy . proteinuria in nephritis, spirometry in asthma and creatinine kinase in myositis. Therapy should be tapered off. For example, with prednis(ol)one, the dose is reduced in steps of -5 mg every 3-7 days down to 15 mg/day. At that point, switch to alternate day therapy and reduce in mg steps over 2-3 weeks. This minimises the impact on mood and lessens the drop in general well-being.