What is it about?

We utilized in silico analyses to show that 25 GAD sequences from human gut bacterial sources show sequence and motif similarities to human β cell GAD65. Our motif analyses determined that most gut GAD sequences contain the pyroxical dependent decarboxylase (PDD) domain of human GAD65, which is important for its enzymatic activity. Additionally, we showed relevant motifs and T cell epitope overlaps with known human GAD65 T cell receptor epitopes, which may implicate the immune destruction of β cells. Thus, we propose a physiological hypothesis in which changes in the T1D gut microbiome result in a release of bacterial GAD, thus causing miseducation of the host immune system. Due to the notable similarities, we found between human and bacterial GAD, these deputized immune cells may then target human β cells leading to T1D development.

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Why is it important?

First instance of this correlation


Novel approach to connecting the gut dysbiosis and autoimmune diabetes (T1D).

Monica Westley PhD
Vanderbilt University

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This page is a summary of: Similarities between bacterial GAD and human GAD65: Implications in gut mediated autoimmune type 1 diabetes, PLoS ONE, February 2022, PLOS,
DOI: 10.1371/journal.pone.0261103.
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