A 3D rendering of Borrelia burgdorferi bacteria, which cause Lyme disease. Image: Hydra/Adobe Stock
Borrelia burgdorferi, the bacterium that causes Lyme disease, infects nearly half a million individuals in the United States annually, and many more worldwide. While most people who become infected with this tick-borne pathogen fully recover with antibiotics, others experience chronic Lyme disease. These patients suffer arthritic and neurologic symptoms for months to years, even after antibiotic treatment.
Michael Starnbach, PhD, a professor of microbiology in the Blavatnik Institute at Harvard Medical School, is using single-cell sequencing techniques to profile immune responses to B. burgdorferi infection in samples from mice and patients with Lyme disease. Large-scale computational approaches and artificial intelligence tools have helped Starnbach and his colleagues demonstrate that, during infection, immune cells (specifically T cells) are manipulated by B. burgdorferi in ways that severely impair their ability to resolve infection.
The Starnbach Lab has developed methods to restore, in a mouse model of B. burgdorferi infection, the capacity of T cells to clear B. burgdorferi and resolve associated pathologies. To enhance immunity, the lab has tested existing drugs—immune system checkpoint inhibitors developed by colleagues at Harvard—and pioneered novel strategies to reprogram T cells to resist manipulation by B. burgdorferi.
“At the same time, we are finding that these approaches are also helpful in resolving another tick-borne human disease, babesiosis,” Starnbach says.
This vital research has been driven by the generous support of Emily and Malcolm Fairbairn, MBA ’94, who have given more than $6 million to support a range of promising research initiatives at HMS aimed at deepening understanding of Lyme disease and its profound impact on patients. “Our continued dedication is driven by the belief that this work will help patients restore their vitality and well-being,” says Emily Fairbairn.