Primary Research Focus
The Savinov Lab focuses on studying the underlying mechanisms controlling organ-specific autoimmune diseases such as type I diabetes (T1D). Progression of T1D involves the activation of autoimmune T cells, consequent homing of activated lymphocytes to the pancreatic islets, and ensuing destruction of insulin-producing beta cells.
Pathogenesis of type I diabetes (T1D) is driven by continuous destruction of insulin-producing β cells within the pancreatic islets, performed directly by autoreactive islet-specific T lymphocytes. The Savinov Lab current research projects are focused on the mechanisms involved in the regulation of T cell activation and tolerance in regard to T1D, even though most of them could take place in other autoimmune processes. Using genetic mouse models, and variety of primary and established cell lines, we are examining the molecular mechanisms leading to inefficient negative co-stimulation, a control mechanism for T cell activation by auto-antigens, along with some defects in the intracellular signaling cascades involved in the autoimmune process.
By determining how autoimmune T cells are initially activated during T1D pathogenesis, how they home to the target organ and how they destroy their beta cell targets, causing clinical onset of T1D, the Savinov Lab hopes to find an effective molecular therapy capable of controlling the autoimmune process.
About the Savinov Lab
Lab Projects and News
Is the heterogenic mother mitochondrial DNA genome a cause of reject in transplanted organs from cloned animals?
This is an investigation to understand if the use of organs from cloned animals in organ transplantation, specifically nuclear-mitochondrial incompatibilities, leads to organ rejection when organs from cloned animals are used for treating end-stage disease.
Genetic Regulation of Human Beta Cell Destruction
This research focuses on elucidating the mechanistic implications for the contribution of T1D-associated allelic variants during the activation and effector phases of CTL function.