Our research is driven by a fundamental question: why do some tumor-specific CD8+ T cells eliminate cancer while others, despite recognizing the same tumor, fail?
We study the intrinsic programs that distinguish successful tumor-rejecting T cells—from how they recognize tumor antigens, become activated, and migrate, to how they maintain function within the suppressive tumor microenvironment.
By comparing T cells with dramatically different antitumor outcomes, we have uncovered previously unrecognized regulators of CD8+ T-cell function. Our recent work reveals that a T cell's ability to reach and effectively engage and kill its target is not simply a consequence of conventional measures of activation/cytotoxicity, but is actively controlled by intrinsic molecular programs governing migration, adhesion and immunological synapse formation.
In parallel, we investigate how neoepitope quality and tumor immune visibility determine whether an immune response ultimately translates into tumor rejection, and how these vulnerabilities can be therapeutically exploited.
Our goal is not simply to describe dysfunctional T cells. We want to understand what makes the successful ones different—and use that knowledge to engineer better antitumor immunity.
By combining functional immunology with CRISPR screening and engineering, single-cell genomics, TCR analysis, proteomics, immunopeptidomics, and in vivo tumor models, we move from fundamental mechanisms to therapeutic strategies designed to make tumor-specific T cells reach better, function better, and persist longer.