https://www.sciencedirect.com/science/article/abs/pii/S0952791522000346

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.

https://doi.org/10.1016/j.coi.2022.102187Get rights and content

Highlights

•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.

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