Abstract
Lyme disease, caused by Borrelia burgdorferi, is transmitted to humans by Ixodes ticks. CCL17 is a potent chemokine that plays important roles in diverse illnesses, including autoimmune and infectious diseases. CCL17 knockout mice, infected with B. burgdorferi, had a reduced pathogen load in the heart compared to control animals. Mice lacking CCL17 also showed signs of immune alteration upon B. burgdorferi infection, including diverse serum levels of proinflammatory cytokines and less monocytes and macrophages infiltration. CCL17 also interacts directly with B. burgdorferi, the first demonstration that this chemokine has an affinity for a vector-borne pathogen.
