@Article{ecn.2009.0179,
AUTHOR = {Anneleen Berende, Marije Oosting, Bart-Jan Kullberg, Mihai G. Netea, Leo A. B. Joosten},
TITLE = {Activation of innate host defense mechanisms by <i>Borrelia</i>},
JOURNAL = {European Cytokine Network},
VOLUME = {21},
YEAR = {2010},
NUMBER = {1},
PAGES = {7--18},
URL = {http://www.techscience.com/ECN/v21n1/65874},
ISSN = {1952-4005},
ABSTRACT = {<i>Borrelia</i> is the causative agent of Lyme disease, a widespread disease with important health conse-quences.
Immune-mediated mechanisms are believed to play a major role in both host defense and in late com-plications
of Lyme disease. Recognition of <i>Borrelia</i> 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 <i>Borrelia</i>: 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 <i>Borrelia</i> recognition, but little is known about other
CLRs such as dectin-1. After PRRs have recognized <i>Borrelia</i>, a signaling cascade is induced that leads to tran-scription
of NF-κB, 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.},
DOI = {10.1684/ecn.2009.0179}
}