Our lab focuses on a select group of cancer types, with a strong emphasis on non-small cell lung cancer, high-grade serous ovarian cancer, glioblastoma, and melanoma. We develop murine model systems that accurately replicate clinically relevant phenotypes and use comparative models to investigate why immune responses fail to control tumors.
Dendritic cells are rare but essential for detecting diseased cells through specialized receptors that sense danger. We aim to understand how interactions between dendritic cells and cancer cells influence the cells’ ability to stimulate an immune response.
Dendritic cells play a crucial role in communicating detected threats to T cells. They migrate to the lymph nodes, where they interact with T cells in an antigen-specific manner. These early interactions are essential for shaping the functional capacity of the T cell response and, ultimately, the ability to control the tumor.
Lymph nodes serve as communication hubs that tailor immune responses to the specific needs of the organs they drain. We study how different lymph node environments are established and how these localized conditions either suppress or promote anti-tumor immune responses.
Within the tumor, T cells must frequently interact with stimulatory myeloid cells to sustain their effector function. These interactions are spatially coordinated by chemokine gradients. We aim to identify which myeloid populations are best suited for stimulatory interactions and which ones suppress anti-tumor immunity.
To therapeutically modify immune responses, we are exploring checkpoint blockade immunotherapy, cytokine therapy, peptide and mRNA-based immune stimulation, and innovative immune-engineering approaches to enhance anti-tumor immunity. Our studies aim to uncover the mechanisms behind each therapeutic intervention’s effectiveness, accelerating translation and therapeutic development.
After their initial activation, T cells differentiate and acquire effector functions or other traits that enable them to eliminate cancer cells, survive within the tumor microenvironment, or persist in lymphoid organs as memory cells. We aim to understand how dendritic cell-derived signals and therapeutics influence T cell fate.
For T cells to effectively control tumors, they must be recruited into the tumor microenvironment. This process is guided by chemokine gradients, often established by dendritic cells within the tumor. We study how specific environments, tumor contexts, and immune cell populations influence T cell infiltration and distribution.