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. Author manuscript; available in PMC: 2014 Mar 1.
Published in final edited form as: Trends Endocrinol Metab. 2013 Jan 8;24(3):109–119. doi: 10.1016/j.tem.2012.11.005

Figure 4.

Figure 4

Glucocorticoids promote the resolution of inflammation and restore homeostasis. Glucocorticoids affect nearly every cell type by virtue of nearly ubiquitous expression of the glucocorticoid receptor (GR). During the course of inflammation, glucocorticoids are able to promote resolution by repressing the expression of adhesion molecules, preventing rolling adhesion and extravasation of neutrophils. Glucocorticoids also induce the expression and secretion of Annexin-1, which is able to induce apoptosis of neutrophils at the site of inflammation. Prolonged glucocorticoid exposure induces tissue resident macrophages (MΦ) to undergo a phenotypic change to become M2-like or anti-inflammatory. These macrophages no longer produce proinflammatory cytokines. Instead they produce interleukin-10 (IL-10), have enhanced phagocytic activity to remove apoptotic cells, and promote tissue healing. Glucocorticoids also act on naïve and differentiated T cells that have been recruited to the inflammatory site by blocking T helper 1 (Th1)- and Th2-derived cytokine production as well as inducing apoptosis.