2025 PRESENTER PROFILES
Innovative Cellular and Tolerogenic Therapies in Type 1 Diabetes
Sunday, June 22, at 1:30 p.m. CT
Room W196 BC • McCormick Place Convention Center
Induction of T-Cell Exhaustion for Treatment of Type 1 Diabetes

Paolo Serafini, PhD
Associate Professor,
University of Miami
What is your presentation about?
T cell exhaustion is a natural mechanism that helps maintain immune homeostasis, primarily through the interaction of PD-1 on T cells with its ligand PD-L1. While blocking this tolerogenic pathway has led to major breakthroughs in cancer immunotherapy, the opposite approach—enhancing exhaustion—could have a transformative impact in autoimmune diseases like type 1 diabetes. In my presentation, I will discuss the use of bifunctional RNA therapeutics designed to specifically target mouse and human beta cells in vivo, driving localized PD-L1 expression. This strategy should promote exhaustion selectively in diabetogenic T cells, while sparing T cells with other specificities, thereby preserving overall immune function.
How do you hope your presentation will impact diabetes research or care?
I hope that through this presentation, the discussion, and follow-up interactions, we can better understand what is required to effectively induce exhaustion in diabetogenic T cells in vivo. Beyond promoting immune tolerance, I’m introducing a new class of therapeutics that enables temporally controlled, targeted biological modifications of beta cells with minimal off-target effects. In addition to blocking autoimmunity, we are also advancing programs aimed at enhancing human beta cell proliferation and resistance to apoptosis. This platform of targeted RNA-based therapeutics can be adapted by other groups to address various beta cell needs, ultimately contributing to the broader development of precision therapies for type 1 diabetes.
How did you become involved with this area of diabetes research or care?
I am an immunologist specializing in the study of tolerogenic mechanisms in both cancer and type 1 diabetes. These two fields represent mirror images of immune dysfunction: in cancer, we aim to restore immune activity, while in autoimmune diseases, such as type 1 diabetes, we work to suppress it. My involvement in diabetes research developed from this parallel; by understanding how immune tolerance is disrupted or maintained in cancer, we can apply those insights to autoimmunity, and vice versa. This cross-disciplinary perspective not only deepens our understanding of immune regulation but, when combined with advances in targeted nanotechnology, will help us develop safer and more effective therapies for both diseases.