Mentor: Michael Kennedy, Ph.D.

Type 1 diabetes (T1D) is a genetic autoimmune disease in which the immune system mistakenly attacks and destroys insulin-producing pancreatic β-cells. Development of T1D requires a mutation in the human leukocyte antigen (HLA) gene complex, which is responsible for coding the major histocompatibility complex (MHC) receptors on antigen presenting cells. However, not all genetically predisposed individuals end up developing the disease, indicating T1D is likely triggered by external factors. Studies have indicated a link between human gut microbiota and T1D progression. More specifically, Parabacteroides distasonis has been shown to share an epitope with the insulin β-chain, which indicates a potential for bacterial peptide molecular mimicry. Additionally, a correlation has been observed between T1D progression and “leaky” gut syndrome, indicating that the thinning of the mucosal lining in the intestine potentially plays an important role in the gut microbiota's ability to trigger disease development. Thus, leading to the potential for both gut microbial dysbiosis and “leaky” gut syndrome being a potential trigger in the development of T1D in genetically predisposed individuals.

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