Our lab is currently using various mouse models and molecular/cellular/omics techniques to study intestinal immune responses toward environmental cues including microbes and food.

We demonstrated how dsRNA from enteric viruses (norovirus, rotavirus, and commensal viruses) are recognized by intestinal epithelial cells-specific Nod-like recpetors-Nlrp6 and Nlrp9, and activate inflammasome and interferon (PNAS, 2024; Cell, 2021; Nature, 2017a; Science, 2015); and also sensed by DC-expressed Rig-I to sustain the expansion of intraepithelial lymphocytes (Nature Immunology, 2019).

Our lab elucidated that the dietary-antigen-dependent cleavage of Gasdermin D maintains food toleranceirrespective of pyroptosis (Cell, 2023); and found amino-acid formula induces microbiota dysbiosis and depressive-like behavior in mice(Cell Reports, 2024).

Our lab has also investigated the potential immune mechanisms that contribute to microbiota dysbiosis (Cell Research, 2022; PNAS, 2021), and role of microbiota dysbiosis (elevated Clostridium scindens, Peptostreptococcus anaerobius, or Enterococcus faecalis and these bacteria produced metabolites DCA, IDA, or Tyramine) in colorectal cancer or IBD development (Immunity, 2024; Nature Cell Biology, 2024; Cell Host Microbe, 2024); we also developed strategies (glucosylated nanoparticle encapsulated antibiotics or vitamin supplementation) to intervene microbiota dysbiosis and associated diseases such as IBD(Nature Biomedical Engineering, 2022; Cell Reports, 2022).