Type 1 diabetes (T1D) is a chronic autoimmune disease characterized by the destruction of pancreatic, insulin-producing beta cells by autoreactive T-cells. Limited research is available on what activates autoreactive T-cells though T1D incidence is increasing worldwide. People with T1D have altered gut microbiome which is thought to be associated with T1D development. In T1D, amino acids 9-23 of the insulin B chain (insulin B:9-23) are a primary autoantigen. We previously showed Parabacteroides distasonis (Pd), a human gut commensal, has a peptide in HPRT that cross-reacts with human and mouse insulin B:9-23-specific T-cells in vitro. Orally gavaging 3-week non-obese diabetic (NOD) mice with Pd accelerated diabetes onset compared to the saline-treated mice. We hypothesize Pd is accelerating T1D onset via molecular mimicry of insulin B:9-23. Pd did not stimulate small intestinal epithelial lymphocytes and did not change small and large intestinal permeability.  The abundance of only 28 amplicon sequence variants changed, indicating gut alpha diversity was minimally affected. Among the cytokines, Pd colonization lowered IL-15. Injecting mice with the metabolite most enriched in colonized mice, TMAO, did not significantly accelerate pancreatic insulitis. To assess the impact of Pd in the absence of gut microbes, germ-free NOD mice were orally gavaged with Pd once at 3 weeks of age. Germ-free NOD Pd-colonized mice had more severe insulitis but gut permeability and the serum metabolite composition did not change. Neonatal NOD mice gavaged with Pd, had fewer splenic CD4+ T-cells, more FOXP3+ regulatory T-cells, suggesting immune tolerance to Pd. Our findings further support our hypothesis that Pd accelerates T1D onset via insulin mimicry. Despite enhancing a specific autoimmune response, Pd causes similar effects as non-inflammatory commensals in NOD mice.