NIH Research Festival
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Autoimmune disorders arise when the immune system mistakenly targets and damages the body's own tissues. Molecular mimicry, where foreign antigens resemble host cell receptors, is a proposed mechanism triggering autoimmune responses. We aim to explore whether molecular mimicry contributes to autoimmune diseases affecting the human thyroid gland. Previous research suggests certain bacteria in the human microbiota may share immunological similarities with thyroid tissue, potentially contributing to the development of thyroid autoimmune disorders. Specifically, we hypothesize that proteins in extracellular vesicles (EVs) released by these bacteria have sequence homology to B and T cell epitopes of thyroid proteins. To investigate this hypothesis, we isolated EVs from three strains of bifidobacterium and conducted proteomic analysis of both EVs and bacterial cells using mass spectrometry. Our analysis aims to identify bacterial and EV proteins with sequence homology to autoimmune epitopes of thyroid proteins. In further experiments, we will conduct biolayer interferometry (BLI) studies to assess the binding affinities between bacterial EVs and thyroid autoantibodies. Understanding the role of the microbiome, particularly bacterial EVs, in autoimmune thyroid disorders could lead to novel diagnostic and therapeutic approaches. This research contributes to elucidating the complex interplay between microbial components and autoimmune pathogenesis in the thyroid gland.
Scientific Focus Area: Immunology
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