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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 

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Glucocorticoid signaling: a nongenomic mechanism for T-cell immunosuppression.

Glucocorticoids were long believed to exert their effects through transcriptional regulation of glucocorticoid-receptor target genes. However, there is accumulating evidence for nongenomic glucocorticoid-receptor-dependent modulation of signal transduction pathways. Here, we review rapid glucocorticoid activities and focus on a novel mechanism that underlies nongenomic glucocorticoid-induced immunosuppression in T cells. The findings demonstrate a physical and functional interaction between the glucocorticoid receptor and the T-cell receptor (TCR) complex. In its unligated state, the glucocorticoid receptor has an important role in TCR signaling but, after glucocorticoid-receptor-ligand binding (caused by short-term treatment with the synthetic glucocorticoid dexamethasone), the TCR complex is disrupted, leading to impaired TCR signaling. These data reveal a dichotomal functional role for glucocorticoid receptors: one in the cytosol as part of the TCR complex and the other as a nuclear regulator of gene transcription. Drugs that selectively target membrane-bound glucocorticoid receptors might represent a novel immunosuppressive approach.[1]

References

  1. Glucocorticoid signaling: a nongenomic mechanism for T-cell immunosuppression. Löwenberg, M., Verhaar, A.P., van den Brink, G.R., Hommes, D.W. Trends. Mol. Med (2007) [Pubmed]
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