After moving to the United States from Russia, I pursued a career as a researcher at the University of Pittsburgh with a primary focus on the initial applications in preclinical murine models of dendritic cell-based vaccines for immunotherapy of cancer. The focus of my current research is exploration of the immunomodulatory approaches that would allow rectification of the migratory patterns of the Treg cells in the murine model of T1D.

This builds on my previous research addressing immunomodulatory approaches for therapy of Type 1 Diabetes. I established a model in which long term physiologically adequate function of the autologous β cells was recovered in non-obese diabetic (NOD) mice after onset of hyperglycemia by rendering them hemopoietic chimerae. These mice were termed antea-diabetic. In the following study the role of T regulatory (Treg) cells in mechanisms mediating these events was addressed and generated data demonstrated that (i) expression of Foxp3 and Treg cell-associated chemokine molecules are compromised in unmanipulated NOD mice of different ages with the most profound effect detected in the pancreatic lymph nodes (PLN); and that (ii) restraint of autoimmunity and restoration of euglycemia observed in antea-diabetic mice was associated with an increase of Foxp3 transcripts in the PLN, exceeding their normal levels. In light of the evidence that physiologically sufficient recovery of the autologous β cells could be achieved by suppressing autoimmunity associated with normalization of the Treg cells population in the PLN, an immunomodulatory regimen aimed at refining trafficking of Treg cells into the PLN might become a new therapeutic approach for Type 1 Diabetes.

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