IMMUNOLOGY2025™ Conference Recordings-T cell epitope spreading from microbial to autoantigens

T cell epitope spreading from microbial to autoantigens

Video Transcription

Video Summary

James Moon explains two related studies on how autoimmune disease may begin through epitope spreading and, possibly, molecular mimicry. In post-infectious antibiotic-refractory Lyme arthritis, his team used immunopeptidomics and T-cell/antibody assays to identify self-antigens in joint tissue, including fibronectin, laminin, and collagen, and found immune reactivity mainly in the refractory Lyme group. They also found some Borrelia peptides that resembled these self-epitopes, though tetramer data did not definitively prove cross-reactive T cells.<br /><br />In a rheumatoid arthritis project, the group focused on gut commensals associated with RA, especially specific strains of Ochromonas and Ruminococcus. They identified bacterial peptides presented in synovial tissue and found T-cell and antibody responses, again strongest in RA patients with evidence of microbial IgA coating. The talk concludes with plans to build better mouse and microbiome models to directly test cross-reactivity and tolerance failure in autoimmunity.

Keywords

epitope spreading

molecular mimicry

autoimmune disease

Lyme arthritis

rheumatoid arthritis

immunopeptidomics