Presenting Author: Xin Chen
, postdoc at Stanford Univ. Sch. of Med.
Abstract:
Post-Treatment Lyme Disease (PTLD) is characterized as a persistent inflammatory condition in a large fraction of patients following antibiotic treatment for Borreliella infection, but what leads to PTLD is not known. Here, we analyzed 56 peripheral blood mononuclear cell (PBMC) samples from 23 individuals at risk for PTLD in a multi-year longitudinal study via single-cell RNA sequencing. We found a significant association between an expanded subset of pro-inflammatory monocytes and Lyme disease, a phenomenon notably more prevalent in PTLD patients compared to individuals who have returned to health (RTH). Furthermore, PTLD patients exhibited a range of autoimmune-related phenotypes, absent in healthy and RTH individuals, including a positive correlation between disease severity and CD8+ KIR+ Tregs, functional impairment of CD4+ FOXP3+ Tregs, and heightened lymphocyte cytotoxicity. Interestingly, these phenotypes are associated with the stimulation by a specific peptidoglycan produced by Borreliella and this may be a key driver of PTLD. These findings hold significant potential for the development of targeted therapeutic strategies for PTLD, potentially transforming patient prognosis.
A distinct autoimmune signature in Post-treatment Lyme Disease Syndrome (PTLD)
Category
Poster and Podium (Block Symposium)
Description
Custom CSS
double-click to edit, do not edit in source
Date: May 5 Presentation Time: 03:15 PM to 04:30 PM Room: Exhibit Hall F1