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CUTTING EDGE |
*
Department of Pathology, University of Utah School of Medicine, Salt Lake City, UT 84132;
Institute for Medical Microbiology and Immunology, Technical University of Munich, Muenchen, Germany; and
Tularik, Inc., South San Francisco, CA 94080
The agent of Lyme disease, Borrelia burgdorferi,
produces membrane lipoproteins possessing potent inflammatory
properties linked to disease pathology. The recent association of
toll-like receptors (TLR) 2 and 4 with LPS responses prompted the
examination of TLR involvement in lipoprotein signaling. The ability of
human cell lines to respond to lipoproteins was correlated with the
expression of TLR2. Transfection of TLR2 into cell lines conferred
responsiveness to lipoproteins, lipopeptides, and sonicated B.
burgdorferi, as measured by nuclear translocation of NF-
B
and cytokine production. The physiological importance of this
interaction was demonstrated by the 10-fold greater sensitivity of
TLR2-transfected cells to lipoproteins than LPS. Futhermore,
TLR2-dependant signaling by lipoproteins was facilitated by CD14. These
data indicate that TLR2 facilitates the inflammatory events associated
with Lyme arthritis. In addition, the widespread expression of
lipoproteins by other bacterial species suggests that this interaction
may have broad implications in microbial inflammation and
pathogenesis.
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