Ye Zheng earned his B.S. from Peking University in Beijing, China, and his Ph.D. from Columbia University. He was awarded a postdoctoral fellowship by the Cancer Research Institute to conduct research in Alexander Rudensky’s lab at the University of Washington in Seattle. After a brief sojourn as a research scholar at Memorial Sloan Kettering Cancer Center, he joined the Salk Institute for Biological Studies in 2009.

Regulatory T cells (Tregs) are a specialized subset of T cells that play a critical role in suppression of overexuberant immune response and maintenance of immune system homeostasis. Abnormal Treg function has been linked to multiple autoimmune diseases, such as arthritis, type 1 diabetes, lupus and multiple sclerosis, as well as inefficient tumor immunity. Research in the Zheng lab is focused on the molecular and cellular mechanisms of regulatory T cell development and function in the context of autoimmune and metabolic diseases. Foxp3, a member of the forkhead transcription factor family, is expressed specifically in regulatory T cells, and plays a pivotal role in Treg development and function. The Zheng lab discovered an intronic enhancer, named CNS2, at the Foxp3 genomic sequence, which is a “signal hub” for protection of Treg identity. They found that the activation of Tregs is a key event that triggers CNS2:promoter looping activity to stabilize Foxp3 expression. In addition to Tregs’ role in preventing autoimmune diseases, the Zheng lab recently revealed that Tregs are also involved in the development of metabolic diseases. They demonstrated that accumulation of adipose tissue resident Tregs is associated with insulin resistance in aged mice. This study highlighted a novel role of the immune compartment in contributing to key aspects of adipose health and disease.