The first line of defense
Innate immunity is promptly activated after microbial infection to initiate protective responses through the production of inflammatory cytokines from various immune cells. These cells express various pattern recognition receptors (PRRs) which recognize signature molecules of the pathogen (PAMPs). We focus on understanding these mechanisms to explore how they trigger the induction of inflammatory cytokines for host defense.
Current research highlights
Cytosolic DNA sensor IFI16 is essential for the activation of programmed cell death pathways in influenza virus-infected cells. It functions as an RNA sensor for the influenza A virus by interacting with genomic RNA.
Investigating how NIX-mediated mitophagy regulates metabolic reprogramming during mycobacterial infection, leading to macrophage differentiation and resolution of infection.
Comparative transcriptome analysis of SARS-CoV, MERS-CoV, and SARS-CoV-2. We are identifying altered ribosomes and mitochondrial pathways to discover potential drug candidates via repurposing.
Exploring the role of miR-30e in targeting multiple negative regulators of innate immune signaling, and how its sequestering in SLE patients reduces type-I interferon.
Studying how particulate matter enhances RNA virus infection by skewing and suppressing anti-viral innate immunity during Influenza virus infection.
Principal investigator & profiles
Osaka University, Japan