Our mission: Our laboratory in the IBP Department and Center for Immunology focuses on the immune mechanisms controlling cardio-metabolic disease. As obesity is closely associated with chronic inflammation, our goal is to discover the mechanisms by which the immune system regulates networks of inflammatory signaling pathways that ultimately trigger disease.
Our impact: Our research is relevant to public health because obesity results in an increased risk of fatty liver disease, heart failure, coronary artery disease, type 2 diabetes, stroke, and certain types of cancer. Obesity and its complications are among the major health challenges of our time. Our projects provide a deeper understanding of how the immune system regulates metabolic disease and provide diagnostic and therapeutic targets for its prevention and treatment.
Our values: Our main priority is to conduct innovative research with high rigor and reproducibility. We believe it is key to work with humility, authenticity, and have fun while doing science. We are a truly collaborative group as demonstrated in our articles and grants. We strive to provide an inclusive, diverse, and supportive lab environment with high standards for excellence.
Our research projects:
1. Immune mechanisms promoting inflammation and fibrosis during fatty liver disease.
Non-alcoholic fatty liver disease (NAFLD) is estimated to affect 30% of the population and is a leading cause of abnormal liver function. NAFLD covers a wide spectrum of liver pathology ranging from fatty liver to non-alcoholic steatohepatitis (NASH), characterized by steatosis, inflammation, hepatocellular injury, and fibrosis. Our studies utilize state-of-the-art approaches to identify the triggers of inflammation in fatty liver disease, which is a major need in the field. We focus on the role of B cells and macrophages in the pathogenesis of disease. This work is funded by an R01 award entitled “Mechanisms of B Cell Pathogenicity in Non-Alcoholic Fatty Liver Disease”.
2. Immune mechanisms regulating cardiac remodeling in heart failure.
Cardiovascular disease and heart failure are leading causes of death. Recently, the focus has shifted towards cardiomyocyte-extrinsic mechanisms involving cardiac immune cells. Monocyte-derived macrophages and T cells have been identified as critical for the progression to heart failure. Our goal is to identify immune mechanisms that regulate physiological and pathological cardiac remodeling. Our central hypothesis is that cardiac resident macrophages promote compensatory remodeling during cardiac stress following crosstalk with B cells. This work is funded by a MPI R01 award entitled “Immune Mechanisms Regulating Cardiac Remodeling”.
3. Immune mechanisms maintaining intestinal homeostasis in diet-induced obesity.
The intestinal immune system is emerging as an important modulator of obesity-associated metabolic disorders. However, the mechanisms by which intestinal immune cells influence the development of obesity and how the obese state affects gut immune homeostasis are unclear. Our long-term goal is to identify immune mechanisms that regulate intestinal inflammation in the obese gut. The Peyer’s patches (PPs) are gut-associated lymphoid tissues distributed throughout the small intestine and are the major source of IgA-producing B cells. In the PPs, T follicular helper (TFH) cells support affinity maturation of B cells in the germinal center and their class-switch to IgA+ plasma cells. Our current work aims to determine how obesity causes a disruption of TFH cell homeostasis