My research focuses on how metabolic regulation within the tumor microenvironment affects the anti-tumor immunity of T cells. Our goal is to develop metabolic strategies to combat cancer. We have provided evidence supporting the role of metabolic activity in cancer immunotherapy, demonstrating that tumor-associated metabolism is influenced by infiltrating T cells— a concept we refer to as "immunometabolic editing." (Cell metabolism 35:118, Jan 2023)

Building on our previous findings published in Nature Immunology (21:298, 2020) and incorporating insights from other studies, we identified CD36 as a potential target for enhancing current cancer immunotherapies. Targeting CD36 may promote T cell activity while reducing the presence of immune-suppressing FoxP3+ regulatory T cells. To this end, we developed a humanized anti-CD36 antibody and demonstrated its therapeutic effects in a mouse model of liver cancer, where it prevented CD8 T cell exhaustion and rejuvenated the stemness of CD8+ T cells (Cancer Discovery 15:1676 2025 ).

These studies aim to open new avenues in tumor immunology, offering fresh perspectives on the design of metabolism-altering treatments that could influence immune checkpoint blockade therapies in hepatocellular carcinoma (HCC) and other malignancies. Our findings will serve as a foundation for future investigations into how metabolic signals modulate the connection between metabolism and immunity.

We are currently expanding our research to include various types of cancer, such as prostate and lung cancer, as well as kidney disease. Our approach involves integrating spatial transcriptomics, multiplex immunohistochemistry, spectral flow cytometry, and genetic mouse models. In addition to these methods, we are also exploring metabolic approaches and cell-based therapies for the treatment of these diseases.