Type 1 diabetes (T1D) is a genetic autoimmune disease in which the immune system mistakenly attacks insulin-producing cells, known as β cells. Autoreactive T cells, or killer T cells, are key to the destruction of pancreatic β cells (1). The genetic component of T1D is a mutation found in a gene within the human leukocyte antigen (HLA) complex, which helps the immune system differentiate the body’s proteins from foreign proteins (1, 2). Although this genetic component is established, only about 5% of individuals with the mutation ultimately develop T1D (2). Since T1D does not strongly correlate with this mutation, environmental factors are likely at play.
The gut microbiome is composed of many microbes. Two of the major phyla that are found in the gut are Firmicutes and Bacteroidetes. There have been previous studies that indicate a relationship between the gut microbiome and T1D, but this relationship is not fully understood (3). Individuals without this autoimmune disease have a mucus layer that prohibits bacteria from entering the epithelium. The effects T1D has on the mucus layer are also not fully understood (4). It is hypothesized that Parabacteroidetes distasonis shares an epitope with human insulin and likely has a role in T1D development (3). Another possibility is that T1D causes a change in the thickness of the mucosal layer that lines the intestines, allowing bacteria to access the epithelial layer.