Lyme disease, an infection caused by the bacterium Borrelia burgdorferi transferred via tick bite, affects some 300,000 people in the US each year. In most cases, patients are treated with a 2- to 3-week course of antibiotics, and recover without lasting problems. But a small number of affected people experience long-term symptoms of arthritis despite treatment, and findings from a new study conducted at University of Utah Health suggest why this happens. The research identified a mechanism that activates T cells, triggering the production of inflammatory molecules that contribute to inflammation and arthritis. Study first author Sarah Whiteside, a graduate student at U of U Health, commented, “We believe that in this model persistent Lyme arthritis is a result of [overactive] immune response.” The findings were published online earlier this week in Journal of Immunology.
The study identified a receptor on T cells that is affected by B. burgdorferi, resulting in bystander activation. Long after the initial tick bite, these activated T cells produce a cascade of inflammation resulting in infection-induced autoimmunity. While the exact mechanism of activation is still unclear, the findings suggest that therapies that target anti-inflammatory mechanisms may be promising for patients with persistent Lyme arthritis. Janis Weis, PhD, professor of pathology at U of U Health, observed, “If you can suppress T cell activation for the short-term, we might help re-establish the control mechanism [for the immune response] in the body.”
Read a news story about the discovery.
The journal abstract may be read here.
Posted on February 6, 2018