Nuclear receptor signalling in dendritic cells connects lipids, the genome and immune function

EMBO J. 2008 Sep 17;27(18):2353-62. doi: 10.1038/emboj.2008.160. Epub 2008 Aug 21.

Abstract

Dendritic cells (DCs) are sentinels of the immune system and represent a heterogeneous cell population. The existence of distinct DC subsets is due to their inherent plasticity and to the changing microenvironment modulating their immunological properties. Numerous signalling pathways have impacts on DCs. It appears that besides cytokines/chemokines, lipid mediators also have profound effects on the immunogenicity of DCs. Some of these lipid mediators exert an effect through nuclear hormone receptors. Interestingly, more recent findings suggest that DCs are able to convert precursors to active hormones, ligands for nuclear receptors. Some of these DC-derived lipids, in particular retinoic acid (RA), have a central function in shaping T-cell development and effector functions. In this review, we summarize and highlight the function of a set of nuclear receptors (PPARgamma, RA receptor, vitamin D receptor and glucocorticoid receptor) in DC biology. Defining the contribution of nuclear hormone receptor signalling in DCs can help one to understand the regulatory logic of lipid signalling and allow the exploitation of their potential for therapeutic intervention in various immunological diseases.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Cell Nucleus / metabolism
  • Dendritic Cells / cytology*
  • Genome
  • Humans
  • Immune System
  • Lipids / chemistry*
  • Models, Biological
  • PPAR gamma / metabolism
  • Receptors, Calcitriol / metabolism
  • Receptors, Cytoplasmic and Nuclear / metabolism*
  • Receptors, Glucocorticoid / metabolism
  • Receptors, Retinoic Acid / metabolism
  • Signal Transduction*

Substances

  • Lipids
  • PPAR gamma
  • Receptors, Calcitriol
  • Receptors, Cytoplasmic and Nuclear
  • Receptors, Glucocorticoid
  • Receptors, Retinoic Acid