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Assessment of Combination Therapy for Type 1 Diabetes (T1D) Progression in NOD Mice
Location: 15
Mentor: Dr. Wasif Khan
Type 1 Diabetes (T1D) affects more than 1.4 million people in the U.S., including 500,000 children, and its incidence is increasing. T1D results from the destruction of the pancreatic beta cells, which produce insulin, resulting in insulin deficiency and hyperglycemia. This consequential hyperglycemia leads to several metabolic disorders and is a leading cause of blindness, amputation, and kidney failure. Although the causes remain unclear, it is well established that T1D results from an autoimmune attack with specificity for pancreatic beta cells. This highly specific autoimmune response indicates a critical role of the T and B cells of adaptive immunity in the pathogenesis of this disease.
We propose the use of a dual therapy, combining a set of drugs that target B and T cells respectively, and are currently being tested in clinical trials. Ibrutinib blocks B cell activity by inhibiting BTK and thus has been demonstrated to restrain the immune response in various mouse models. Concurrently, a fellow lab (Malek) developed a drug targeting Tregs using a fusion protein (mIL-2/CD25) that has limited diabetes progression in numerous animal models. This new drug is also being tested in humans.
To evaluate the efficacy of this dual treatment, female NOD mice were randomly separated into four groups and administered either a monotherapy or combination therapy, with age and company matched NOD mice serving as controls. Histological analysis of pancreatic tissue revealed
The results, discussion, and conclusion - (Results coming soon)
