Campus Only Senior Thesis
Bachelor of Arts
© 2013 Natasha Uday Pabrai
Individuals under 20 years old have the highest risk of developing type 1 diabetes because their beta cells are destroyed at a faster rate than any other age group. Previous studies have looked at delaying and slowing down the rate of beta cell destruction through the use of anti-CD3 antibody treatments. Specifically, Teplizumab and Otelixizumab drug therapies have been used to treat individuals within 12 weeks of diagnosis. Previous studies done with Teplizumab and Otelixizumab have focused on individuals between 12 and 40 years old; however, there is little research done the effects of these treatments on individuals under 12 years old. Since type 1 diabetes is primarily diagnosed in children the purpose of this proposal is to further the knowledge of the preservation of beta cells in children with the use of Teplizumab and Otelixizumab drugs over 2 years. This study will also focus on the delay of onset type 1 diabetes with the use of Teplizumab in high-risk individuals under 20 years of age. The high-risk individuals will be determined by using genetic screening on individuals with an affected immediate family member. Individuals will also be tested to see if they carry insulin autoantibodies (IAA), protein tyrosine phosphate-related IA-2 molecule (IA-2A), islet cell antibodies (ICA), and glutamic acid decarboxylase (GADA). Individuals that test positive for carrying the DR3/DR4 alleles in the genetic screening and that have two or more autoantibodies present in their immune systems will be selected to participate. The purpose of this proposal is to further understand the impact of anti-CD3 antibody treatment on young individuals diagnosed with type 1 diabetes and to further understand if treatment in young individuals with anti-CD3 antibodies can delay or prevent the onset of type 1 diabetes.
Pabrai, Natasha Uday, "The Use of Anti-CD3 Treatment and Genetic Screening to Delay Further Beta Cell Destruction in Type 1 Diabetes" (2013). Scripps Senior Theses. 284.
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