Glucocorticoids and the innate immune system: Crosstalk with the Toll-like receptor signaling network

Toll-like receptors (TLRs) are responsible for the recognition of a variety of microbial pathogens and the initial induction of immune and inflammatory responses. These responses are normally restricted by the adrenally produced glucocorticoid hormones which provide a feedback mechanism to curb unab...

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Bibliographic Details
Published in:Molecular and cellular endocrinology 2007-09, Vol.275 (1), p.30-42
Main Authors: Chinenov, Yurii, Rogatsky, Inez
Format: Article
Language:English
Subjects:
Animals
Glucocorticoid receptor
Glucocorticoids - physiology
Humans
Immunity, Innate - physiology
Innate immunity and inflammation
Interferon regulatory factors
Receptor Cross-Talk - physiology
Receptors, Glucocorticoid - physiology
Signal Transduction - physiology
Toll-like receptors
Toll-Like Receptors - chemistry
Toll-Like Receptors - physiology
Transcription, Genetic - physiology
Transcriptional regulation
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Summary:Toll-like receptors (TLRs) are responsible for the recognition of a variety of microbial pathogens and the initial induction of immune and inflammatory responses. These responses are normally restricted by the adrenally produced glucocorticoid hormones which provide a feedback mechanism to curb unabated inflammation. Glucocorticoids act through a ligand-dependent transcription factor—the glucocorticoid receptor (GR), which engages in a complex network of protein:protein and protein:DNA interactions ultimately activating or repressing target gene transcription. Not surprisingly, multiple mechanisms account for the glucocorticoid interference with TLR signaling including enhanced expression of the natural inhibitors of TLR pathways, direct repression of TLR-activated transcriptional regulators and cross-utilization of cofactors essential for both GR and TLR signaling. Here we discuss recent and unexpected examples of crosstalk between the two transcriptional networks and the emerging role of GR in the regulation of innate immunity.
ISSN:0303-7207
1872-8057
DOI:10.1016/j.mce.2007.04.014