Millions of people around the world live with type 1 diabetes (T1D), a chronic, incurable autoimmune condition that produces significant acute and long-term health complications. T1D is caused by the destruction of insulin-producing beta cells by immune cells that escape the body’s normal mechanisms for tolerance induction. Our research seeks to develop novel interventions that can effectively eliminate or inactivate this immune cell-mediated autoimmune attack on pancreatic beta cells, thereby establishing a new, curative therapy for T1D. Our experimental approach engages the body’s natural pathways for specific tolerance induction and has shown promise for preventing T1D initiation in a mouse model of beta cell autoimmunity. In this QFASTR Development project, we will test whether our strategy can additionally halt ongoing beta cell destruction and rescue diabetes pathology at later stages of the disease – after the onset of immune infiltration of the pancreas and potentially even after the emergence of overt clinical symptoms. Successful completion of this work has the potential to validate a new, targeted approach to re-establish and sustain immune tolerance as an effective clinical therapy for T1D and autoimmunity more broadly.

Funding

Funding Duration

July 1, 2026 - June 30, 2028

People

Principal Investigator

Amy Wagers

PhD
Forst Family Professor of Stem Cell and Regenerative Biology, Faculty of Arts & Sciences, Harvard University
Co-PI
Collaborators