Figure 2.

A classical model of GR-mediated inflammatory repression. First, cytoplasmic GR interacts with glucocorticoids, resulting in a conformational change and nuclear translocation. A, primary repression resulting from GR monomers tethering to inflammatory transcription factors, such as NF-κB, leading to recruitment of corepressors. B, GR homodimers interact with specific DNA sequences, also resulting in recruitment of corepressors and reduced transcription of inflammatory genes. C, secondary repression resulting from GR homodimers inducing the transcription of genes encoding proteins that repress inflammatory gene transcription, such as NFKBIA.