IMMUNOLOGY2026™ Conference Recordings For Attendees-Persistent Microbial Peptidoglycan Drives Post-Infectious Autoimmunity in Lyme Disease

Persistent Microbial Peptidoglycan Drives Post-Infectious Autoimmunity in Lyme Disease

Video Transcription

Video Summary

Xin Chen presented evidence that post-treatment Lyme disease may involve autoimmune-like immune dysregulation driven by persistent Borrelia peptidoglycan. Single-cell sequencing of patient blood found increased Th17 cells, inflammatory T-cell signatures, reduced suppressive markers in regulatory T cells, and a unique hyperinflammatory monocyte population linked to symptoms. In healthy monocytes, Borrelia peptidoglycan triggered inflammatory pathways overlapping with, but distinct from, LPS, and produced gene signatures resembling autoimmune disease. Using a human immune organoid system, the team showed peptidoglycan-activated monocytes could promote autoreactive B-cell responses more strongly than LPS. The work suggests chronic exposure to bacterial peptidoglycan may help drive post-infectious autoimmunity or autoinflammation in Lyme disease, and possibly other diseases as well.

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Date April 19, 2026 10:30 AM - 10:45 AM

Room 153 AB

Session Primary Immune Deficiency and Immune Dysregulation

Speaker Xin Chen

Track Immune Mechanisms of Human Disease (HUM)

Year 2026

Keywords

post-treatment Lyme disease

Borrelia peptidoglycan

autoimmune-like immune dysregulation

Th17 cells

single-cell sequencing

April 19, 2026 10:30 AM - 10:45 AM

153 AB

Primary Immune Deficiency and Immune Dysregulation

Xin Chen

Immune Mechanisms of Human Disease (HUM)

2026