The Weyand Lab
The immune system is critical for host defense against cancer and infections but is also the key driver of immune-mediated disease. CD4+ T cells are the carriers of immune memory, their cytokines orchestrate protective and pathogenic immunity, and they function as helper cells to regulate other immune cell subsets. Monocytes/macrophages are the “soldiers” of the immune system, engulf pathogens and apoptotic cells, secrete immune effector molecules and digest tissue. Dependent on the signals they receive, monocytes/macrophages adopt pro- and anti-inflammatory phenotypes. In autoimmune disease, the immune system fails to protect and instead causes chronic inflammatory tissue injury. The Weyand lab focuses on immune system abnormalities in three autoimmune diseases, studying patients with rheumatoid arthritis (RA), medium and large vessel vasculitis (LVV) and coronary artery disease (CAD). The lab employs cutting-edge imaging technologies, genomics and a humanized mouse model to dissect molecular pathways in individual human cells and in human tissues. We identify complex biomarkers of autoimmunity and our near-term goal is the development of novel therapies. Our group is highly diverse in scientific interest, career status and geographic origin. We celebrate diversity and love to work together.
Our scientific focus areas
T cell immunometabolism
Exploring how nutrient sensing and bioenergetic strategies guide T cell function. The lab investigates how CD4 T cells from rheumatoid arthritis patients use fuel sources, generate metabolites, regulate the glycolytic machinery, co-ordinate mitochondrial function and produce biosynthetic precursors.
Immuno-protection of blood vessels
Defining mechanisms through which healthy blood vessels guard against inflammation. Our scientists investigate how defects in immunoregulation and abnormalities in vascular cells induce leakage and breakdown of the immunoprivilege in medium and large arteries, e.g. the aorta. Our favorite disease is giant cell arteritis (GCA) which causes blindness, stroke, aortic arch syndrome, and aortic aneurysms.
Examining how metabolically re-programmed macrophages mediate tissue damage in RA, vasculitis, and atherosclerosis. The program aims to understand which environmental cues misdirect cell-intrinsic metabolic pathways and how metabolites participate in immune-stromal interactions.
Identifying molecules protecting and de-protecting telomeric ends as telomeric damage triggers premature aging of T cells and forces their functional deviation towards pro-inflammatory effector cells. The project studies the DNA damage machinery in T cells from RA patients and the functional consequences of imprecise repair.