Gut microbe peptide implicated in triggering type 1 diabetes
Type 1 diabetes (T1D) is an autoimmune disease characterized by the destruction of pancreatic -cells. One of the earliest aspects of this process is the development of autoantibodies and T cells directed at an epitope in the B-chain of insulin (insB:9–23). Analysis of microbial protein sequences with homology to the insB:9–23 sequence revealed 17 peptides showing >50% identity to insB:9–23. Finally, analysis of human children's guts microbiome data from a longitudinal DIABIMMUNE study revealed that seroconversion rates (i.e., the proportion of individuals developing two or more autoantibodies) were consistently higher in children whose microbiome harbored sequences capable of producing the hprt4–18 peptide compared to individuals who did not harbor it. Taken together, these data demonstrate the potential role of a gut microbiota-derived insB:9–23-mimic peptide as a molecular trigger of T1D pathogenesis.