Abstract Text: Lyme disease (LD) is caused by Bacteria Borrelia and is transmitted through a bite of an infected tick. LD has become the most prevalent tick-borne disease in North America. LD usually can be treated by antibiotics, but still, around 20% of LD patients develop chronic joint inflammation (arthritis), fatigue, and musculoskeletal pain which is characterized as Post-Treatment Lyme Disease Syndrome (PTLD). Therefore, PTLD has been suggested to be triggered by an autoimmune response but how the immunological reality of PTLDs is not well known. In this work, we identified an increase of CD8+ Tregs as we found in various autoimmune diseases. Importantly, we also identified a population of inflammatory CD14+ monocytes dominant in PTLD patients, compared to return-to-health patients and healthy patients through single cell sequencing analysis. This monocyte cluster displayed distinct inflammatory gene signatures such as CCL3, CCL4, IL1B, CXCL2, CXCL8, and others. Similar inflammatory macrophages have been observed recently in RA, and so both these results firmly place Lyme disease in the realm of autoimmunity, which has not been very clear previously. Tracking this inflammatory monocyte subset could lead to a more accurate prediction of PTLD and identify molecular biomarkers and pathways for therapeutic intervention.
