From Benign Autoimmunity to Type 1 Diabetes: a Misguided Dialogue between T Cells and Beta Cells

Summary: Type 1 diabetes (T1D) is classically viewed as an autoimmune disease. While this certainly still holds true, recent work by us and others have highlighted a universal state of “benign” autoimmunity present in all individuals. The key question is therefore to understand the mechanisms by which this benign autoimmunity progresses towards an aggressive state and leads to T1D. Two non-mutually exclusive mechanisms are at play: defective immune regulation and an increased vulnerability of beta cells to the autoimmune attack. These mechanisms also provide relevant therapeutic targets that we are exploring in preclinical mouse and in-vitro human models and in patients. Overall, T1D should now be viewed as both an autoimmune and a beta-cell disease, and should be treated accordingly.

Biography: R. Mallone received his MD PhD degree from the University of Turin, Italy. After a Postdoc with Jerry Nepom at the Benaroya Institute in Seattle, he moved to Paris where he is currently Professor of Immunology at Université Paris Cité, Diabetologist at the Cochin Hospital and leads a research team at the INSERM Cochin Institute. He is also director of a satellite research lab at the Indiana Biosciences Research Institute in Indianapolis. His research spans from preclinical studies with human samples and mouse models to clinical trials. It focuses on autoimmune T cells and their dialogue with pancreatic beta cells to understanding type 1 diabetes mechanisms and develop novel biomarkers and therapeutics.