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

Nat Rev Immunol. 2010 May;10(5):365-76. doi: 10.1038/nri2748.


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.

Publication types

  • Review

MeSH terms

  • Animals
  • Humans
  • Inflammation / immunology*
  • Liver X Receptors
  • Macrophages / immunology*
  • Nuclear Receptor Co-Repressor 1 / physiology*
  • Nuclear Receptor Co-Repressor 2 / physiology
  • Orphan Nuclear Receptors / physiology
  • PPAR gamma / physiology
  • Receptors, Cytoplasmic and Nuclear / physiology*
  • Receptors, Glucocorticoid / physiology
  • Repressor Proteins / physiology*
  • T-Lymphocytes / immunology*
  • Transcriptional Activation


  • Liver X Receptors
  • NCOR1 protein, human
  • Nuclear Receptor Co-Repressor 1
  • Nuclear Receptor Co-Repressor 2
  • Orphan Nuclear Receptors
  • PPAR gamma
  • Receptors, Cytoplasmic and Nuclear
  • Receptors, Glucocorticoid
  • Repressor Proteins