20 years RIG-I

Prof. Takashi Fujita from the Institute of Virus Research at the university of Bonn, Prof. Mitsutoshi Yoneyama from the Research Institute of Disaster Medicine at the Chiba University and Prof. Hiroki Kato from the Institute of Cardiovascular Immunology at the University Hospital in Bonn now published a collaborative review article in celebration of 20 years after the discovery of RIG-I. The article delves into the captivating realm of RIG-I research, exploring the advancements made over the past two decades. Published in the latest edition of "Immunity," the review sheds light on the critical role of Retinoic Acid-Inducible Gene I (RIG-I) receptors in the innate immune system.

Recognized as pattern recognition receptors (PRRs), RIG-I receptors play a crucial role in detecting viral RNA and initiating antiviral responses. Their discovery in the early 2000s revolutionized virology research, positioning RIG-I receptors as vital targets for therapeutic intervention against viral infections. Moreover, their involvement in autoimmune diseases, cancer immunotherapy, and vaccine development underscores their broad significance in biomedical research.

Summary

The RIG-I like receptor (RLR) is 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 RLR and the mechanism of sensing non-self RNA are described. Usually, self-RNA is refractory to RLR; however, there are underlying host mechanisms that prevent immune reactions. Studies have revealed that the regulatory mechanisms of RLR 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.