Troy Krahl

TL;DR: Results show that diabetes induced by Coxsackie virus infection is a direct result of local infection leading to inflammation, tissue damage, and the release of sequestered islet antigen resulting in the re-stimulation of resting autoreactive T cells, further indicating that the is let antigen sensitization is an indirect consequence of the viral infection.

TL;DR: It is demonstrated that the Th2 cytokine IL-4 can prevent the development of autoimmunity and destructive autoreactivity in the NOD mouse and its ability to regulate the disease process in the periphery indicates that autoimmune diabetes in NOD mice is not a systemic disease, and it can be modulated from the islet compartment.

TL;DR: It is proposed that cells infected with RDAd vectors present antigens for recognition by class 1 major histocompatibility complex-restricted cytotoxic T lymphocytes by a mechanism that does not require viral replication or de novo protein synthesis.

TL;DR: The results suggest that a costimulatory signal by CD40L is required early but not in the effector phase of disease development, and conclude that CDL-CD40 costimulation is required for early events in the development of spontaneous autoimmune diabetes.

TL;DR: The data demonstrate polarization of chemokine expression by Th1 vs Th2 cells, which, within the microenvironment of the pancreas, accounts for distinctive inflammatory infiltrates that determine whether insulin-producing beta-cells are protected or destroyed.