Retinoid X receptor α attenuates host antiviral response by suppressing type I interferon

Feng Ma, Su-Yang Liu, Bahram Razani, Neda Arora, Bing Li, Hiroyuki Kagechika, Peter Tontonoz, Vanessa Núñez, Mercedes Ricote and Genhong Cheng ()
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Feng Ma: Immunology, and Molecular Genetics, University of California
Su-Yang Liu: Immunology, and Molecular Genetics, University of California
Bahram Razani: Immunology, and Molecular Genetics, University of California
Neda Arora: Immunology, and Molecular Genetics, University of California
Bing Li: University of California
Hiroyuki Kagechika: Institute of Biomaterials and Bioengineering, Tokyo Medical and Dental University
Peter Tontonoz: Howard Hughes Medical Institute
Vanessa Núñez: Centro Nacional de Investigaciones Cardiovasculares (CNIC)
Mercedes Ricote: Centro Nacional de Investigaciones Cardiovasculares (CNIC)
Genhong Cheng: Immunology, and Molecular Genetics, University of California

Nature Communications, 2014, vol. 5, issue 1, 1-12

Abstract: Abstract The retinoid X receptor α (RXRα), a key nuclear receptor in metabolic processes, is downregulated during host antiviral response. However, the roles of RXRα in host antiviral response are unknown. Here we show that RXRα overexpression or ligand activation increases host susceptibility to viral infections in vitro and in vivo, while Rxra−/− or antagonist treatment reduces infection by the same viruses. Consistent with these functional studies, ligand activation of RXR inhibits the expression of antiviral genes including type I interferon (IFN) and Rxra−/− macrophages produce more IFNβ than WT macrophages in response to polyI:C stimulation. Further results indicate that ligand activation of RXR suppresses the nuclear translocation of β-catenin, a co-activator of IFNβ enhanceosome. Thus, our studies have uncovered a novel RXR-dependent innate immune regulatory pathway, suggesting that the downregulation of RXR expression or RXR antagonist treatment benefits host antiviral response, whereas RXR agonist treatment may increase the risk of viral infections.

Date: 2014
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DOI: 10.1038/ncomms6494

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