Activation of innate host defense mechanisms by
Borrelia.

Eur Cytokine Netw. 2010 Mar 1;21(1):7-18.

Activation of innate host defense mechanisms by Borrelia.

Berende A, Oosting M, Kullberg BJ, Netea MG, Joosten LA.

Department of Medicine, Radboud University Nijmegen Medical
Center, Nijmegen, Nijmegen Institute for Infection, Inflammation
and Immunity (N4i), Department of Internal Medicine, Jeroen Bosch
Hospital, 's Hertogenbosch, The Netherlands.

Borrelia is the causative agent of Lyme disease, a widespread
disease with important health consequences. Immune-mediated
mechanisms are believed to play a major role in both host defense
and in late complications of Lyme disease.
Recognition of Borrelia and the initial activation of the innate
immune system are important for host defense, as well as
modulation of adaptive responses.
Several classes of pattern recognition receptors (PRRs) have been
suggested to be involved in the recognition of Borrelia:
Toll-like receptors (TLRs), NOD-like receptors (NLRs) and C-type
lectin receptors (CLRs). TLR2 has been found to be the most
important receptor of the TLRs. The intracellular receptor NOD2,
a member of the NLRs, might also play an important role in
recognition. Mannose receptor is also involved in Borrelia
recognition, but little is known about other CLRs such as
dectin-1. After PRRs have recognized Borrelia, a signaling
cascade is induced that leads to transcription of NF-kappaB,
resulting in the production of pro-inflammatory cytokines.
Understanding these pathways provides not only a better insight
into the pathogenesis, but also provides potential, novel,
therapeutic targets during active disease or post-infection
complications.

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PMID: 20146985 [PubMed - in process]