Every year, more than 300,000 Americans contract Lyme disease, an infection caused by Borrelia burgdorferi, a bacterium transferred during a tick bite. In a small percentage of patients, infection symptoms, including arthritis, persist despite antibiotic treatment.
Scientists at University of Utah Health believe they identified a mechanism that activates T cells, a key component of the immune system, which could explain the elusive link between a tick bite and persistent Lyme arthritis. The results are published online in the February 5th issue of 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.
