Type 1 diabetes (T1D) is caused by the destruction of pancreatic b-cells via an autoimmune response. T-cells and autoantibodies are known to target insB:9-23 peptide, an epitope of the insulin B-chain. According to a recent study, a gut bacterial peptide that mimics insB:9-23 can accelerate T1D development in non-obese diabetic (NOD) mice. Researchers found 17 microbial peptides with greater than 50% identity to insB:9-23.
Among them, hprt4-18 peptide from a bacterium activated T-cell hybridomas from NOD mice and T-cell clones from T1D patients. In addition, when NOD mice were colonized with the bacterium, an increased number of macrophages, CD8+T cells, dendritic cells, and decreased levels of FoxP3+ regulatory T cells were observed. Furthermore, a higher proportion of autoantibody development (seroconversion rate) was found in children with a microbiome that can produce hprt4-18…
