Physiological functions of RIG-I-like receptors

Mitsutoshi Yoneyama; Hiroki Kato; Takashi Fujita

doi:10.1016/j.immuni.2024.03.003

Physiological functions of RIG-I-like receptors

Immunity. 2024 Apr 9;57(4):731-751. doi: 10.1016/j.immuni.2024.03.003.

Authors

Mitsutoshi Yoneyama¹, Hiroki Kato², Takashi Fujita³

Affiliations

¹ Division of Molecular Immunology, Medical Mycology Research Center, Chiba University, Chiba, Japan; Division of Pandemic and Post-disaster Infectious Diseases, Research Institute of Disaster Medicine, Chiba University, Chiba, Japan.
² Institute of Cardiovascular Immunology, Medical Faculty, University Hospital Bonn, University of Bonn, Bonn, Germany.
³ Institute of Cardiovascular Immunology, Medical Faculty, University Hospital Bonn, University of Bonn, Bonn, Germany; Laboratory of Regulatory Information, Institute for Frontier Life and Medical Sciences, Kyoto University, Kyoto, Japan. Electronic address: fujita.takashi.86e@st.kyoto-u.ac.jp.

PMID: 38599168
DOI: 10.1016/j.immuni.2024.03.003

Abstract

RIG-I-like receptors (RLRs) are crucial for pathogen detection and triggering immune responses and have immense physiological importance. In this review, we first summarize the interferon system and innate immunity, which constitute primary and secondary responses. Next, the molecular structure of RLRs and the mechanism of sensing non-self RNA are described. Usually, self RNA is refractory to the RLR; however, there are underlying host mechanisms that prevent immune reactions. Studies have revealed that the regulatory mechanisms of RLRs involve covalent molecular modifications, association with regulatory factors, and subcellular localization. Viruses have evolved to acquire antagonistic RLR functions to escape the host immune reactions. Finally, the pathologies caused by the malfunction of RLR signaling are described.

Keywords: CARD; LGP2; MAVS; MDA5; RIG-I; autoimmunity; innate immunity; interferon; non-self RNA; virus.

Publication types

Review

MeSH terms

DEAD Box Protein 58
DEAD-box RNA Helicases* / genetics
Immunity, Innate
Interferon-Induced Helicase, IFIH1 / metabolism
RNA
Receptors, Immunologic
Signal Transduction*

Substances

DEAD-box RNA Helicases
Interferon-Induced Helicase, IFIH1
DEAD Box Protein 58
Receptors, Immunologic
RNA