Shilpa Sachan, Nicole Baumgarth
Lyme disease is caused when mammalian hosts not part of the sylvatic life cycle, including humans, are infected with Borrelia burgdorferi (Bb) following the bite of an Ixodes tick. Ticks and natural mammalian host reservoirs, including rodents, however, are largely disease tolerant, despite Bb establishing persistent infection. We explore the complex and ongoing interplay between Bb and the immune system. We discuss how Bb infection-induced innate responses seem maladapted to this extracellular bacterial infection, perhaps explaining why CD4+ T cells are ineffective contributors to Bb infection control. While B cell responses critically control Bb tissue burden and disease development they cannot clear the infection, showing a bias towards ongoing plasmablast responses and a lack of functional germinal centers. Identifying the mechanisms that hinder effective immune clearance of Bb may lead to new approaches for the treatment of Lyme Disease.