Translational type 1 diabetes pathobiology; beta-cell biology, pancreatic islet biology, apoptosis; insulin secretion; cytokines; signal transduction; endoplasmic reticulum (ER) stress; diabetes models; systems biology; disease gene prediction, post-translational modifications of antigens, neoepitopes in type 1 diabetes.

My prime aim is to understand type 1 diabetes (T1D) pathogenesis at the molecular and cellular level. The overall working hypothesis is that part of the genetic component underlying T1D is caused by variation in beta-cell-expressed genes having functional effects such as regulation of apoptosis, proliferation, and insulin secretion. By multifaceted clinical and molecular approaches, we aim to identify causal T1D risk genes and validate their functional roles in loss- and gain-of-function studies in relevant model systems. The perspective is that increased knowledge of the genes and biological processes causing T1D can be used to more accurately predict T1D risk, increase prognostic efficacy, and to optimize and individualize treatment strategies.

None.

Immuno diabetology; translational research; cell biology; molecular biology; diabetes models; inflammatory processes