Cited by 619Nuclear Receptors and SignalingEstrogen and related hormone effectsPsoriasis: Treatment and Pathogenesis

Nuclear receptor transrepression pathways that regulate inflammation in macrophages and T cells

Glass, Christopher K., Saijo, Kaoru·2010·Nature Reviews Immunology

Abstract

Members of the nuclear receptor superfamily of ligand-dependent transcription factors regulate diverse aspects of immunity and inflammation by both positively and negatively regulating gene expression. Here, we review recent studies providing insights into the distinct mechanisms that enable nuclear receptors to antagonize pro-inflammatory programmes of gene expression in macrophages and T cells by altering the turnover or recruitment of co-repressors and co-activators in a gene-specific manner. These nuclear receptor-dependent transrepression pathways are proposed to have roles in controlling the initiation, magnitude and duration of pro-inflammatory gene expression and are amenable to pharmacological manipulation.

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Crossref · 10.1038/nri2748

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References 84 · Cited by 619

Authors
Glass, C. K., & Saijo, K.
Affiliations
University of California San Diego (US)
Corresponding author
Glass, Christopher K.
Venue
Nature Reviews Immunology
Published
2010-05
Volume
10
Issue
5
Pages
365-376
ISSN
  • 1474-1733 (ISSN-L)
  • 1474-1741
OpenAlex
W2002762124
Cited by
619
References
84
Citations by year
2026: 27 · 2025: 20 · 2024: 19 · 2023: 18 · 2022: 28 · 2021: 34 · 2020: 28 · 2019: 36 · 2018: 39 · 2017: 49 · 2016: 40 · 2015: 48 · 2014: 57 · 2013: 60 · 2012: 62
FWCI
5.08
Type
journal article
Language
en
Open access
closed
Locations
  • Nature reviews. Immunology (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Nuclear Receptors and Signaling
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Genetics › Estrogen and related hormone effects
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
Keywords
nuclear receptors, transrepression, inflammation, macrophages, microglia, Th17 cells, corepressors, transcriptional coactivator, pro-inflammatory gene expression, transcriptional regulation, T helper cell differentiation, pharmacological manipulation
MeSH terms
Liver X Receptors, Animals, Humans, Inflammation, Macrophages, Receptors, Glucocorticoid, Repressor Proteins, T-Lymphocytes, Transcriptional Activation, Receptors, Cytoplasmic and Nuclear, PPAR gamma, Nuclear Receptor Co-Repressor 1, Nuclear Receptor Co-Repressor 2, Orphan Nuclear Receptors

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