Research

Research Overview

Regulatory T (Treg) cells are central to the maintenance of immune tolerance, yet their function extends far beyond the prevention of autoimmunity. We investigate how Foxp3⁺ Treg cells integrate immune and metabolic signals to preserve tissue homeostasis—and how their dysfunction drives autoimmune and metabolic disease.

Research Focus

We view the Treg cell compartment as a dynamic and heterogeneous system rather than a uniform suppressive population. Our work has established that thymus-derived (tTreg) and peripherally induced (pTreg) cells represent functionally distinct lineages that cooperate to maintain immune equilibrium, but can diverge in their roles across tissues and disease contexts.

A central theme of our research is how Treg cell specialization is shaped by local microenvironments. In metabolic tissues such as visceral adipose tissue, Treg cells acquire tissue-adapted phenotypes that are essential for controlling inflammation and maintaining systemic metabolic balance. Disruption of these programs—including the destabilization and transdifferentiation of Treg cells—can actively drive chronic inflammation and disease progression.

Beyond immune regulation, we explore emerging roles of Treg cells in tissue repair, regeneration, and metabolic control, highlighting their broader function as integrators of organismal homeostasis.

Future Directions

Our goal is to define the molecular logic that governs Treg cell fate, stability, and functional specialization across tissues. We aim to leverage this knowledge to develop targeted strategies for restoring immune tolerance, including the design of antigen-specific and tissue-adapted Treg cell therapies for autoimmune and metabolic diseases.