Hui-Ming Chen

Deciphering How Dysregulated Emergency Myelopoiesis Drives Disease Progression and Immune Resistance

Our laboratory investigates how dysregulated emergency myelopoiesis reshapes myeloid cell development and immune function, and defines its pivotal role in cancer progression, immunosenescence, and immune resistance. We propose that immune resistance arises not only from dysfunction of terminally differentiated myeloid cells but also from aberrant myelopoiesis.
Persistent dysregulation of emergency myelopoiesis disrupts both intramedullary and extramedullary myelopoiesis, driving the excessive expansion of immunosuppressive monocytes and dysfunctional antigen-presenting cells, leading to an immunosuppressive microenvironment that compromises host immune surveillance and limits the efficacy of immunotherapy.

Beyond disease-associated mechanisms, the regulatory networks governing pathological myelopoiesis are among the key determinants of immune remodeling and therapeutic responsiveness.

Our research focuses on myeloid immune checkpoints, particularly the Siglec family, to elucidate how they regulate myelopoiesis and peripheral myeloid cell function. By integrating fundamental mechanistic studies, botanical drug discovery, and clinical translation, we have established a comprehensive research platform aimed at reprogramming pathological myeloid immunity and developing next-generation precision immunotherapies.