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B cells, splenic marginal zone, and complement -as opsonin and inflammatory mediator- in the immunopathogenesis of virally induced Type 1 Diabetes


Approximately 150 million people are affected with diabetes mellitus worldwide. One form of diabetes, Type I diabetes, is an autoimmune disease that accounts for about 10% of all cases. It is mediated by T cells of the immune system that turn against the host (autoreactivity), and specifically destruct insulin-producing beta-cells of the pancreas. The resulting lack of insulin leads to chronic elevated blood sugar, and ultimately contributes to blindness, amputation, renal disease, and premature death.

Both genetic and environmental factors play a role in the development of Type I diabetes. Two widely used rodent models emulate aspects of human disease: while the NOD mouse strain is genetically susceptible and develops disease spontaneously, the RIP-LCMV transgenic mouse model requires an external stimulus, i.e. viral infection, to develop diabetes. This grant application contains a proposal to pursue clues from both literature and preliminary experiments that certain immunological factors (i.e. complement, B c ells, the marginal zone), normally associated with the NOD system, might also influence virally induced diabetes development. Defining shared immunological aspects between the two models could help further clarify the immunopathogenicity of human Type I diabetes.

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