People respond in different ways to Lyme disease, and some of that variation may be influenced by genetics. One area researchers are studying involves TLR1, a gene that plays a role in how the immune system recognizes bacteria, including Borrelia burgdorferi, the bacterium that causes Lyme disease.
A new study published in the journal Frontiers in Immunology from Dr. Klemen Strle’s lab at Tufts University found that people with a specific TLR1 genetic variation tended to have stronger inflammation during early infection, and that this inflammation may persist. This heightened inflammation is linked to a greater risk of arthritis that can persist even after antibiotic treatment. Importantly, this research shows an association between TLR1 variation and increased inflammation, not a direct cause, and more studies are needed to fully understand the role of TLR1 and other genes in Lyme disease outcomes.
“Evidence emerging from this study helps clarify why some patients continue to experience long-term symptoms while others recover more quickly, pointing to differences in immune response rather than the infection alone”, said Dr. Armin Alaedini, GLA’s chief scientific officer. “Research into immune-system genetics”, he added, is “central to understanding the biological drivers of prolonged inflammation.” Although further research is needed, work in this area is steadily refining our understanding of why Lyme disease outcomes differ and how care may one day be individually tailored.
Publication: Williams, M. A., Hernandez, S. A., Arvikar, S. L., Sulka, K. B., Strle, F., Wells, C. C., Petnicki-Ocwieja, T., Steere, A. C., & Strle, K. (2025). Toll-like receptor 1 polymorphism is associated with impaired immune tolerance, dysregulated inflammatory responses to Borrelia burgdorferi, and heightened risk of post-infectious Lyme arthritis. Frontiers in immunology, 16, 1711765. https://doi.org/10.3389/fimmu.2025.1711765
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