Journal of Leukocyte Biology Myeloid cells, immune suppression, tumor immunology
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A more recent version of this article appeared on August 1, 2007

Published online before print February 21, 2007
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© by The Society for Leukocyte Biology
Journal of Leukocyte Biology, doi:10.1189/jlb.1206741

Received for publication December 20, 2006.
Revised January 30, 2007.
Accepted for publication February 1, 2007.

Article

Innate immune system regulation of nuclear hormone receptors in metabolic diseases

Edward Kai-Hua Chow *, Bahram Razani {dagger}, and Genhong Cheng *{ddagger}{sect}@

*Molecular Biology Institute, {ddagger}Department of Microbiology, Immunology and Molecular Genetics, {sect}Jonsson Comprehensive Cancer Center, {dagger}Medical Scientist Training Program, David Geffen School of Medicine, University of California Los Angeles, Los Angeles, California, USA

@ To whom correspondence should be addressed. E-mail: genhongc{at}microbio.ucla.edu.


  Abstract

The immune system modulates a number of biological processes to properly defend against pathogens. Here, we review how crosstalk between nuclear hormone receptors and the innate immune system may influence multiple biological functions during an immune response. Although nuclear hormone receptor repression of innate immune responses and inflammation has been well studied, a number of new studies have identified repression of nuclear hormone receptor signaling by various innate immune responses. IFN regulatory factor 3, a key transcription factor involved in the induction of antiviral genes, may play a role in mediating such crosstalk between the innate immune response and nuclear receptor-regulated metabolism. This crosstalk mechanism is now implicated in the pathogenesis of atherosclerosis and Reye’s syndrome and could provide an explanation for other pathogen-associated metabolic and developmental disorders.

Key Words: innate immunity • metabolism • IRF3 • RXR{alpha}




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