Cancer poses one of the most significant and persistent challenges to our immune system, representing a major threat to human health. Understanding the intricate biology of how our immune system monitors tissues and mobilizes responses against malignant cells, and reciprocally how tumors exploit various strategies to evade immune surveillance, is crucial for advancing cancer treatment.

Recent breakthroughs in elucidating and modulating T cell function—highlighted by the discovery of co-stimulatory and co-inhibitory molecules and the clinical success of immune checkpoint inhibitors and engineered T cells—have profoundly transformed the landscape of cancer immunotherapy. Despite these advances, the heterogeneity of cancer and the emergence of resistance mechanisms frequently result in limited response rates and treatment relapses in a significant number of patients.

From a tissue biology perspective, our laboratory employs a multidisciplinary approach, integrating advanced imaging techniques, immune profiling, and genetic models to decode the fundamental mechanisms underlying immune response initiation from lymphoid organs to tissues. We investigate the development and functional coordination of immune cells from central lymphoid organs, such as the bone marrow and thymus, to peripheral lymphoid organs, including lymph nodes and spleen, and finally to peripheral tissues. Additionally, we explore how tumor development and chronic viral infections disrupt these processes.

A particular focus of our research is the interplay between Myeloid cells and T cells (the Myeloid-T axis) within the tumor microenvironment and related lymphoid structures. We concentrate on dendritic cells (DCs), the principal antigen-presenting cells, and tumor-associated macrophages (TAMs), which play a pivotal role in shaping the tumor’s immune microenvironment. Our goal is to understand how these cells’ functions are influenced by tumor initiation and progression and, in turn, how they affect T cell activity.

Furthermore, in the current immunotherapy era, we recognize that the principles of mechanism of action (MOA) and pharmacology for macromolecular and cellular therapeutics significantly diverge from those of traditional small molecule drugs. This distinction is especially relevant for agonist drugs, where insights from small molecule inhibitors cannot be directly translated. By using cytokine agonists as a model, our lab aims to establish a new paradigm for the development and clinical application of agonistic drugs.