We are broadly interested in how epithelial tissues sense and respond to injury.  

The ability to maintain homeostasis is conserved from unicellular organisms to mammals, which requires sensing and responding to the environment.  Similar to pathogen infection, tissue injury is an ancient and universal insult that disrupts tissue and organismal homeostasis.  Prompt sensing and repair of the injury is essential for organismal health and survival.  While mechanisms of host defense through innate immune sensing of pathogen-derived “non-self” signals have been elucidated, how tissue injury is sensed by the host to coordinate repair is less clear.  

Drawing parallels between pathogen defense and injury repair, our projects focus on:

1) The cellular and molecular mechanisms of injury sensing and repair through innate immune-like signaling pathways.

2) The role of injury-induced signaling in wound-associated malignancy and infection.

3) How local injury regulates organismal homeostasis systemically.  

We use a combination of unique tools we developed in studying innate immune signaling and mouse skin repair including: