Sarah L. Gaffen, PhD

The immune system strikes a tight balance between controlling infections while still limiting immunity to self tissues (‘autoimmunity’). A case in point is T cell derived cytokines: while critical for protecting against infectious disease, they are also central to driving pathology in most autoimmune conditions. Consequently, ‘biologic’ drugs that neutralize cytokines have become mainstays of treating autoimmune diseases. The Gaffen lab takes a basic science approach to understand the molecular and cellular mechanisms that underline cytokine-mediated inflammation, whether for good (prevent infections) or bad (promote autoimmune pathology). Our main focus is IL-17, which is produced mainly by T cells and other lymphocytes. We study IL-17 in antifungal mucosal and systemic host defense, particularly in response to the commensal fungus Candida albicans. In fact, the Gaffen Lab was the first to demonstrate a role for Th17 cells/IL-17 in immunity to mucosal candidiasis, establishing a precedent in the field. We also study cytokine molecular signaling in driving autoimmune and immunopathologic conditions, including rheumatoid arthritis, autoimmune glomerulonephritis, and also other conditions such as graft-versus-host disease in bone marrow transplantation. Recently, we have established a major emphasis on post-transcriptional control of gene regulation, including 'epitranscriptomics' (RNA methylation) and control of protein synthesis at the translational level. We approach these questions using a combination of molecular, cellular, model organism and human/mouse approaches.