Type 1 diabetes (T1D)​ is an organ-specific autoimmune disease characterized by selective destruction of the b ​ cells, the only insulin–producing cells in the body. Like many complex diseases, T1D is influenced by both genetic and environmental factors. Immune dysregulation is key to the pathogenesis of the diseases, but the molecular mechanisms remain incompletely defined and are the subject of intense research.  Mechanistically, T1D is driven mainly by T lymphocytes that respond to b cell-specific antigens, but other types of immune cells, especially innate immune cells, can also have an important role, either enhancing or dampening the autoimmunity. The negative regulators of immune responses are of particular interest due to their potential preventive and therapeutic applications. Meanwhile, immune or environmental insults can influence b​​ cell responses including their survival, the proliferation from the residual cells and the neogenesis from the precursors or other cell types, but how these responses are regulated ​remains​ poorly understood.

We will apply the tools of immunology, genetics, molecular biology and systems biology to understand the pathogenesis of autoimmune diseases, with primary focus on T1D. Specifically, we will study the role of innate immune system, the interactions between innate and adaptive immunity and the underlying mechanisms and signaling pathways.