Abstract
Infection of mice with Borrelia burgdorferi (Bb), a tick-transmitted spirochete and the pathogen that causes Lyme disease in humans, triggers CD4 T cell activation in secondary lymphoid tissues, from which they disseminate into various infected tissues. Despite their activation and the appearance of CD4 T cell-dependent antibody responses, Bb establishes persistent infection in natural Bb reservoir hosts in the absence of overt disease, raising the question of the effectiveness of the anti-Bb T cell responses. Reviewing the existing literature, we propose that CD4 T cells might constitute a host cell target of Bb-mediated immune evasion, rendering these cells ineffective in orchestrating effective inflammatory responses and in supporting highly functional Bb-specific antibody induction. Supporting the induction of more effective CD4 T cell responses may help overcome Bb persistence.