Cited by 133Immune Response and InflammationEstrogen and related hormone effectsReceptor Mechanisms and Signaling

Glucocorticoids and the innate immune system: crosstalk with the toll-like receptor signaling network

Chinenov, Yurii, Rogatsky, Inez·2007·Molecular and Cellular Endocrinology

Abstract

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.

Integrity signals

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Crossref · 10.1016/j.mce.2007.04.014

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153 of 153 references verified0 citation errors · 0 not checkable

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  • Tethering of a GR monomer increases transcription of STAT3, STAT5, CREB, and C/EBP-alpha responsive genes while inhibiting the activity of NF-kappaB, AP-1, ATFs, and IRF3.

    “For instance, tethering of a GR monomer was reported to increase the transcription of STAT3, STAT5, cAMP responsive element binding (CREB), and CCAAT/enhancer binding protein (C/EBP)-α responsive genes while inhibiting the activity of NF-κB, AP-1, activating transcriptions factors (ATFs), and IRF3 (72, 73, 86, 87).”
  • Both composite and tethering GREs enable direct transactivation or transrepression, and the resulting effect on gene transcription is dictated by the transcription factors to which GRs are bound.

    “Interestingly, both composite and tethering GREs enable direct transactivation or transrepression; the resulting effect on gene transcription is dictated by the transcription factors to which GRs are bound.”

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Authors
Chinenov, Y., & Rogatsky, I.
Affiliations
Hospital for Special Surgery (US)
Corresponding author
Rogatsky, Inez
Venue
Molecular and Cellular Endocrinology
Publisher
Elsevier BV
Published
2007-09
Volume
275
Issue
1-2
Pages
30-42
ISSN
0303-7207 (ISSN-L)
OpenAlex
W2060273819
Cited by
133
References
153
Citations by year
2026: 6 · 2025: 7 · 2024: 4 · 2023: 7 · 2022: 9 · 2021: 11 · 2020: 6 · 2019: 6 · 2018: 3 · 2017: 6 · 2016: 9 · 2015: 6 · 2014: 4 · 2013: 7 · 2012: 8
FWCI
3.31
Type
journal article
Language
en
Open access
closed
Locations
  • Molecular and Cellular Endocrinology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Immune Response and Inflammation
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Receptor Mechanisms and Signaling
Keywords
glucocorticoids, Toll-like receptors, innate immunity, glucocorticoid receptor, Toll-like receptor signaling, inflammation, transcriptional regulation, transcriptional cofactors
MeSH terms
Animals, Glucocorticoids, Humans, Immunity, Innate, Receptors, Glucocorticoid, Transcription, Genetic, Signal Transduction, Receptor Cross-Talk, Toll-Like Receptors

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