Immune-mediated diseases such as lupus or rheumatoid arthritis are not caused by an isolated insult resulting in a single dysfunctional gene or pathway, but rather a systemic dysregulation of multiple genes and pathways. Our group uses methods in bioinformatics, and human genetics, and human immunology to better understand the critical elements of dysregulation within the immune system that results in human diseases. We are specifically interested in gene discovery, fine-mapping disease alleles, and integrative functional genomics of autoimmune diseases.
Our group focuses particularly on rheumatoid arthritis, type I diabetes, and tuberculosis. We are interested in (1) using genomics and genetics to identify germline and somatic mutations that predispose to immune-mediated diseases, (2) using those same mutations to identify common pathways, biological processes, and cell-types that play a key role in disease predisposition, and (3) defining the role of those systems within immune cells. For each of these broad goals, the group heavily emphasizes statistical and computational methods.
NRB Building, Room 250, 255
77 Avenue Louis Pasteur
Boston, MA 02115