Every year, more than 300,000 Americans contract Lyme disease, and for a small percentage of them, infection symptoms persist despite antibiotic treatment. Now scientists at University of Utah Health believe they have identified the elusive link between a tick bite and persistent Lyme arthritis. The results were published yesterday in the Journal of Immunology.
"We believe that in this model persistent Lyme arthritis is a result of [overactive] immune response," said the study's first author Sarah Whiteside, a graduate student in Janis Weis’s lab at U of U Health.
The researchers identified a receptor on T cells that interacts with molecules on the surface of B. burgdorferi. Like a key fitting into a lock, the receptors join in a process resulting in bystander activation. This activation mechanism triggers the T cell to produce inflammatory molecules that accumulate around the joints and contribute to inflammation and arthritis.
Some of the newly 'turned-on' T cells can interact with residual bacteria that persists long after the initial tick bite, producing a cascading cycle of inflammation that could lead to infection-induced autoimmunity.
"Through bystander activation, a whole repertoire of T cells may be activated, independent of their specificity for infecting pathogens," explained Weis, professor of pathology.
Whiteside cautions the exact mechanism of T cell activation needs clarification, but the results from this study suggest new therapeutic approaches, such as focusing on anti-inflammatory mechanisms, might be more effective for patients with persistent Lyme arthritis. "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," Weis added.
Image: Analysis of joint tissue reveals reactive and thickened synovium covering the tendon sheath. Image courtesy of Sarah Whiteside.