2000 Summer Research: Latasha King


The Role of Chemokine Gene Polymorphisms in Juvenile Diabetes Susceptibility

Juvenile, or type 1 diabetes is an autoimmune disease. It destroys the body's pancreatic islet cells that produce insulin, which regulates the distribution of glucose to the body's muscles. Patients replace this insulin by daily injections, but still suffer from complications that can lead to blindness, kidney failure and injuries capable of ultimately inducing amputation. Predicting susceptibility and understanding the biology behind disease onset will aid in identifying patients at risk. Some previously identified genes, have demonstrated the ability to play roles in type 1 susceptibility; however, they do not account for all cases. This project will study two chemokine genes, SCYA17 and SCYA22, as candidate genes that might cause a predisposition to type 1 diabetes. Chemokines are small molecules that control how cells of the immune system traffic in the body. Because of their involvement with the immune system and their location on the Human chromosome sixteen (an area of the genome already thought to contribute to susceptibility), SCYA17 and SCYA22 will be thoroughly studied to determine their involvement with the disease. These chemokine genes will be sequenced from eight different people, six with and two without type 1, to identify any possible polymorphic positions, sites at which one or more individuals have a different nucleotide. On a large collection of DNA samples from families where two or more children have type 1 diabetes, an assessment will be done to determine which allele of the polymorphism the children inherit. If they tend to share alleles for this gene, and it is known they have diabetes, this may mean that these genes or something inherited along with these genes is involved in causing diabetes.