New Findings Illuminate Possible Mechanism of Activation
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.
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