Our Research

The mammalian immune system has evolved both the effector and regulatory immune axes, and it sorts, responds to and clears invading pathogens through pro-inflammatory activity, which can cause damage to the affected tissues, and will eventually have to resolve to allow tissue remodeling and resume physiological homeostasis. The balance between pro-inflammatory and suppressive immune functions are critical for health and survival. During the initiation, progress and resolution of inflammation, the local tissue creates a changing microenvironment for immune cell development. We are interested in the immunomodulatory genetic and environmental factors and how they interact to regulate immune homeostasis.

T cells are activated through their antigen receptor (T cell receptor, TCR), and can differentiate according to their nutrient and cytokine microenvironment to become effectors and/or regulators. The interactions among TCR, cytokine and metabolic signaling pathways orchestrate the T cell immune homeostasis under static, lymphopenic and inflammatory conditions, which are the groundwork of our current research projects:

1. Regulatory T cell development and function:
T cells with regulatory function play pivotal roles in controlling pro-inflammatory responses to self- and foreign antigens, as well as to pathogenic and commensal microorganisms. One of the well-known regulatory T cell populations expresses a signature molecule, the transcription factor Foxp3. Others that are Foxp3 but express high levels of the immunosuppressive cytokine IL-10 also have potent immunoregulatory function. We are investigating signals involved in the TCR, cytokine and nutrient sensing pathways in the development and function of Foxp3+ and Foxp3IL-10+ regulatory T cells.

2. Memory and homeostasis of CD8+ T cells:
CD8+ T cells respond to primary pathogenic antigens, develop immune memory and play critical roles in defending against reinfections. In addition to antigen/TCR interaction, the cytokine IL-4 drives innate memory phenotype, and lymphopenia allows homeostatic proliferation along with a robust memory-like phenotype. We are interested in understanding the difference and similarity of memory T cells generated through different routes and whether we can modulate such immune memory by targeting the TCR, cytokine, and metabolic pathways and/or their interactive networking.

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