Antiviral signaling through retinoic acid-inducible gene-I-like receptors.

Abstract

The innate immune system is essential for the first line of host defense against micropathogens. In virus-infected cells, exposed viral nucleotides are sensed by pattern recognition receptors (PRRs), resulting in the induction of type I interferon. Retinoic acid-inducible gene-I-like receptors (RLRs) are a member of PRRs and are known to be crucial molecules in innate immune responses. Upon viral recognition, RLRs recruit their specific adaptor molecules, leading to the activation of antiviral signaling molecules including interferon regulatory factor-3 and nuclear factor-κB. Mitochondrial antiviral signaling (MAVS) protein is also known as one of the adaptor molecules responsible for antiviral signaling triggered by RLRs. Recent reports have identified numerous intracellular molecules involved in the antiviral responses mediated by RLRs/MAVS. Several viral proteins interfere with the RLR/MAVS signaling, allowing the virus to evade the host defense. In this review, we comprehensively update RLR-dependent antiviral signaling with special reference to the RLRs/MAVS-mediated responses.

• Authors: Tomoh Matsumiya, Tadaatsu Imaizumi, Hidemi Yoshida, Kei Satoh
• Journal: Archivum immunologiae et therapiae experimentalis (Arch Immunol Ther Exp (Warsz)) Vol. 59 Issue 1 Pg. 41-8 (Feb 2011) ISSN: 1661-4917 [Electronic] Switzerland
• PMID: 21234810 (Publication Type: Journal Article, Research Support, Non-U.S. Gov't, Review)

Chemical References

• Adaptor Proteins, Signal Transducing
• Ligands
• MAVS protein, human
• PLAAT4 protein, human
• Receptors, Pattern Recognition
• Receptors, Retinoic Acid
• DEAD-box RNA Helicases

Topics

• Adaptor Proteins, Signal Transducing (metabolism)
• Animals
• DEAD-box RNA Helicases (metabolism)
• Humans
• Immunity, Innate
• Ligands
• Protein Processing, Post-Translational
• Receptors, Pattern Recognition (metabolism)
• Receptors, Retinoic Acid (metabolism)
• Signal Transduction
• Ubiquitination
• Virus Diseases (immunology, metabolism, prevention & control)