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. Author manuscript; available in PMC: 2014 Jan 1.
Published in final edited form as: J Clin Rheumatol. 2013 Jan;19(1):19–29. doi: 10.1097/RHU.0b013e31827d8790

Figure 3. Partial molecular architecture underlying the glucocorticoid-induced antagonism of inflammation [80].

Figure 3

Figure reproduced with permission from Rhen et al. N Engl J Med. 2005;353:1711–1723. ≪Note: permission to be provided upon acceptance≫

Inflammatory pathways are characterized by positive feedback loops (ie, cytokines activate NF-κB, which in turn stimulates the synthesis of more cytokines) and by redundancy (ie, cytokines also activate c-Jun–Fos). The glucocorticoid receptor inhibits these pathways at multiple points by directly blocking the transcription of inflammatory proteins by NF-κB and activator protein 1 and by inducing the expression of anti-inflammatory proteins such as IκB, annexin I, and MAPK phosphatase I. Red lines denote inhibition, and black arrows activation.

COX-2 cyclooxygenase 2; cPLA2α, cytosolic phospholipase A2α; IκB, inhibitor of κB; 5-LOX, 5-lipoxygenase; MAPK, mitogen-activated protein kinase; NF-κB, nuclear factor-κB.