Raghavendra Mirmira, MD, PhD
Professor
The University of Chicago
Featured in the Session: Sexual Dimorphism in Islet Responses in the Setting of Diabetes and Obesity
When
Saturday, June 6
at Wednesday, December 30
Where
356 (Level 3)
Ernest N. Morial Convention Center
What is your presentation about?
This presentation will explore why type 1 diabetes, unlike most autoimmune diseases, shows a male predominance after puberty. Using integrated transcriptomic, proteomic, and single-cell approaches in human islets and preclinical models, we identify a heightened inflammatory and interferon-driven response in male beta cells compared to females. We further show that estradiol signaling suppresses antigen presentation and inflammatory pathways in beta cells, reducing their immune visibility and altering islet-immune interactions. These findings highlight a beta cell-intrinsic mechanism underlying sex-biased disease risk and suggest new avenues for preserving beta cell function in autoimmune diabetes.
How do you hope your presentation will impact diabetes research or care?
This work highlights how cellular stress responses shape immune recognition and disease progression. By identifying estradiol signaling as a pathway that suppresses beta cell immunogenicity, these findings suggest new strategies aimed at preserving beta cell function rather than solely targeting the immune system. Ultimately, this perspective may inform more precise, biology-driven approaches to prevention and early intervention in type 1 diabetes.
How did you become involved with this area of diabetes research or care?
My interest in this area stems from a long-standing focus on beta cell biology and its role in the pathogenesis of type 1 diabetes. Over time, our work has increasingly pointed to the importance of beta cell stress responses in shaping immune interactions, which led us to explore how intrinsic differences—such as those driven by sex—might influence disease susceptibility. This line of research reflects a broader goal of studying diabetes as a disorder of both the immune system and the beta cell.