ArticleThe Journal of clinical investigation2024
Wider recognition and greater understanding of postinfectious, antibiotic-refractory Lyme arthritis.
Article in The Journal of clinical investigation, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed.
- Lessons Unlearned: The Barriers to Lyme Borreliosis Vaccination and the Risk of Repeating History.Vaccines · 2026Article
- Characteristics and Clinical Outcomes of Lyme Arthritis: A Retrospective Study.Open forum infectious diseases · 2026Article
- Infection-Triggered Immune Dysregulation and Immunopathology in Lyme Disease: Mechanisms and Clinical Implications.Journal of clinical medicine · 2026Review
- CD8+ T cell depletion promotes human Tph/Tfh cell proliferation and Sjögren syndrome-like symptoms in PBMC-based humanized mice.JCI insight · 2025Article
- The potential to improve Lyme disease diagnostics through quantification of immunoglobulin class switching patterns.Journal of clinical microbiology · 2025Article
Corrections and comments
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Authors and funding
2 authors.
Funding
Abstract
Lyme disease, caused by Borrelia burgdorferi (Bb), can progress to Lyme arthritis (LA). While most patients with LA respond successfully to antibiotic therapy, a small percentage fail to improve, a condition known as antibiotic-refractory Lyme arthritis (ARLA). While T cell responses are known to drive ARLA, molecular mechanisms for ARLA remain unknown. In this issue of the JCI, Dirks et al. isolated disease-specific Th cells from patients with ARLA residing in Germany. A distinct TCR-β motif distinguished ARLA from other rheumatic diseases. Notably, the TCR-β motif was linked predominantly to HLA-DRB1*11 or 13 alleles, which differed from alleles in patients from North America. It also mapped primarily to T peripheral helper (Tph) cells, as opposed to classical Th1 cells. These findings provide a roadmap explaining how T cell responses necessary for control of an infection can, despite antibiotic therapy, drive a disadvantageous T cell response, resulting in a postinfectious, inflammatory arthritis.
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Registered trials
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