CD4 T cell responses in persistent Borrelia burgdorferi infection
- 1Graduate Group in Immunology, University of California Davis, One Shields Ave, Davis, CA 95616, USA
- 2Center for Immunology and Infectious Diseases, University of California Davis, One Shields Ave, Davis, CA 95616, USA
- 3Department of Pathology, Microbiology, and Immunology, School of Veterinary Medicine, University of California Davis, One Shields Ave, Davis, CA 95616, USA
Available online 9 May 2022, Version of Record 9 May 2022.
- •Multiple immune evasion strategies support B. burgdorferi (Bb) persistent infection.
- •CD4 Th1 polarization correlates with Bb-induced disease not protection.
- •Neither protective Th2 nor Th17 polarization are induced to Bb infection.
- •Strong Tfh induction but impaired T-dependent B cell responses after Bb infection.
- •CD4 T cells may be a host cell target of Bb-induced immune evasion strategies.
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.
- Peer-Reviewed Evidence of Persistence of Lyme:MSIDS copy