Virus infections, such as influenza A epidemic and Chronic Hepatitis C virus infection are still important diseases and outbreaks of newly emerging viruses are serious problems for modern society. Higher animals, including humans, are genetically equipped with mechanisms, collectively known as innate immunity, to counteract viral infections. During the course of replication, many viruses generate double-stranded (ds)RNA, which is virtually absent in normal cells and likely serves as a “foreign molecule” in cells. RIG-I, MDA5 and LGP2, collectively termed as RIG-I-Like Receptors (RLRs) function as sensor for viral dsRNA to initiate production of interferon (IFN) and proinflammatory cytokines (Figure), which block viral replication and promote acquired immunity against viruses. Recently we discovered that persistent activation of MDA5 leads to lupus-like autoimmune disorder in mice. The purpose of our project is to clarify the molecular mechanism underlying the antiviral innate immunity and autoimmunity regulated by RLR, and to develop new diagnostic and therapeutic tools for these diseases. This laboratory belongs to Graduate School of Biostudies.