Type 1 diabetes is the autoimmune-mediated destruction of insulin-producing pancreatic Beta-cells that leads to lifelong insulin therapy. Using the non-obese diabetic (NOD) mouse model which succumbs to type 1 diabetes at a young age, the Serreze lab has identified Nuclear Factor kappa B inhibitor Delta (Nfkbid) as a modulator of disease incidence. Nfkbid-deficient mice demonstrate an accelerated disease onset, despite improved thymic negative selection of autoreactive T cells that is associated with decreases in regulatory T cell populations. My research is focused on understanding molecular mechanisms by which Nfkbid influences regulatory T cell populations in an effort to ultimately develop therapies to halt the autoimmune destruction seen in Type 1 diabetes.
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