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Front Cell Infect Microbiol. 2014 Dec 15;4:175. doi: 10.3389/fcimb.2014.00175. eCollection 2014.

Mechanisms of Borrelia burgdorferi internalization and intracellular innate immune signaling.

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Division of Geographic Medicine and Infectious Diseases, Tufts Medical Center Boston, MA, USA.


Lyme disease is a long-term infection whose most severe pathology is characterized by inflammatory arthritis of the lower bearing joints, carditis, and neuropathy. The inflammatory cascades are initiated through the early recognition of invading Borrelia burgdorferi spirochetes by cells of the innate immune response, such as neutrophils and macrophage. B. burgdorferi does not have an intracellular niche and thus much research has focused on immune pathways activated by pathogen recognition molecules at the cell surface, such as the Toll-like receptors (TLRs). However, in recent years, studies have shown that internalization of the bacterium by host cells is an important component of the defense machinery in response to B. burgdorferi. Upon internalization, B. burgdorferi is trafficked through an endo/lysosomal pathway resulting in the activation of a number of intracellular pathogen recognition receptors including TLRs and Nod-like receptors (NLRs). Here we will review the innate immune molecules that participate in both cell surface and intracellular immune activation by B. burgdorferi.


Borrelia burgdorferi; Lyme disease; Nod-like receptor signaling; Toll-like receptor signaling; endosomal signaling; phagocytosis

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