The fate of developing T cells is determined by the strength of T cell receptor (TCR) signal they receive in the thymus. This process is finely regulated through tuning of positive and negative regulators in thymocytes. Recently, the Family with sequence similarity 49 member B (Fam49b) protein is discovered negative regulator of TCR signaling that has been shown to suppress Rac-1 activity in vitro in cultured T cell lines. However, the contribution of Fam49b to thymic development of T cells is unknown. In our lab, we are focusing on the effect of Fam49b on T cells developing, peripheral survival, and functional activity.
Naive T cells undergo dynamic differentiation and activation to orchestrate adaptive immune responses. While major pathways downstream of the TCR and cytokine receptors are well characterized, the fine-tuning mechanisms that govern STAT3 signaling dynamics during T cell fate decisions remain incompletely understood. In our lab, we focus on identifying novel STAT3 regulators and unraveling key molecular checkpoints that control T cell differentiation and activation.
Chronic inflammation plays a critical role in the development of obesity-associated metabolic disorders such as insulin resistance. Obesity alters the microenvironment of metabolic tissues such as adipose tissue and liver from anti-inflammatory to pro-inflammatory, which promotes low grade systemic inflammation and insulin resistance in obese mice. These inflammatory changes are important because they represent potential therapeutic targets in obesity-induced metabolic disorder as well as obesity. In our lab, we are focusing on the mechanism of obesity-induced systemic inflammation caused by intestinal immune cells and development of novel anti-obesity treatments.
NADPH oxidases (NOX) were initially identified as enzymes involved in immune defense, producing reactive oxygen species (ROS) to eliminate pathogens. These multidomain proteins differ in their requirements for assembly with other proteins and play important roles in regulating ROS production, including the generation of superoxide and hydrogen peroxide. Our lab investigates the molecular mechanisms by which NOX2 generates ROS in macrophages, with the goal of identifying key factors that regulate inflammatory responses in immune cells