Recent success in cancer immunotherapy, including using Chimeric Antigen Receptor (CAR) T cells and immune checkpoint blockade, has demonstrated clearly the power of treating human diseases by modulating the activity of T cells, an important population of white blood cells in humans.

My research interest is to understand the functions of innate-like T cells at the molecular level. These cell types, which share many features in common, include gd T cells, mucosal-associated invariant T (MAIT) cells and invariant natural killer T (iNKT) cells. These T lymphocytes are tissue-homing and have rapid effector functions. They contain expanded populations in all individuals and will not cause graft-versus-host disease when transferred. Therefore, they are potential target populations for treating inflammatory diseases and for stimulating the responses to cancer. By defining the specific mechanisms underlying the unique functions of innate-like T cells, we can put forward new strategies for human immunotherapy.

We have discovered that innate-like T cells exhibit distinct metabolic characteristics, which underlie the important functions of these cells during inflammation. We are interested in deciphering the mechanistic interaction between metabolic remodeling and immune functions in innate-like T cells during the pathogenesis of human diseases, including autoimmune diseases and bacterial infections, in which we have shown that these cells play critical roles.

We take advantage of cutting-edge technologies, including CRISPR-Cas9, novel genetically modified mouse models, metabolomic analysis, and single-cell transcriptomic analysis. The long-term goal of our research is to understand the role of metabolic programs that regulate innate-like T cell responses in human diseases.