Stephan Kissler

Stephan Kissler

Assistant Professor of Medicine
Stephan Kissler

The Kissler lab is studying mechanisms of immune regulation that fail in autoimmunity and in type 1 diabetes in particular.

The lab's research currently focused on two topics. First, we investigate the phenotype and function of regulatory T cells in the pancreas during diabetes pathogenesis. Past research has dealt with genetic determinants of Treg function (e.g. CTLA4 gene variation) and the role of different Treg populations (e.g. pTregs) in autoimmune diabetes. We continue to investigate different aspects of Treg heterogeneity in the NOD mouse model for type 1 diabetes.

Second, we seek to understand the target organ's role in autoimmunity. Pancreatic beta cells that are destroyed by autoimmunity in type 1 diabetes are not mere bystanders. Instead, evidence points to beta cell dysfunction that can trigger or amplify the autoimmune response in the pancreas. We performed the first genome scale CRISPR screen in beta cells to better understand factors that impact beta cell autoimmunity. We are now following up on several promising candidate genes with significant effect on the interaction between immune and beta cells.

With these investigations we strive to devise new therapeutic interventions for the prevention and treatment of this incurable disease. In the process, we hope to improve our fundamental understanding of immune regulation.

Contact Information

Joslin Diabetes Center
Harvard Medical School
1 Joslin Place
Boston, MA 02215
p: 617-309-4071

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