Inhibition of T cell activation by Borrelia burgdorferi

Infection with the spirochete B. burgdorferi induces both innate and adaptive immune responses, which coordinate to control disease progression. Previous studies have demonstrated that Borrelia specific antibodies are critical to the control and resolution of infection. The antibody response is characterized by T cell-independent recognition of numerous B. burgdorferi lipoproteins, which contribute to protection from subsequent challenge. In contrast, the role of T cells in protective vs. disease modulating responses to B. burgdorferi infection is poorly understood. The failure to identify protective T cell epitopes of B. burgdorferi in both mice and humans has limited this line of investigation. We have identified bystander activation of CD4+ and CD8+ T cells during infection, a feature that may obscure the identification of antigen-specific T cell responses. Paradoxically, we have also identified a novel modulatory activity in B. burgdorferi that suppresses activation and proliferation of both CD4+ and CD8+ T cells. Suppression can be demonstrated in naive cells from wild type and SMARTA TCR transgenic mice, indicating the ability to override antigen specific and potentially protective immune responses. Our results are consistent with those of Elsner et al., indicating that B. burgdorferi infection results in temporary immunosuppression of the host. Experiments are ongoing to identify potential molecular mechanisms of suppression.