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Divisions of Pediatric
*
Critical Care and
Infectious Diseases, Ahmanson Department of Pediatrics, Steven Spielberg Pediatric Research Center, Cedars-Sinai Medical Center, and University of California School of Medicine, Los Angeles, CA 90048
Toll-like receptor 2 (TLR2) and TLR4 play important roles in innate
immune responses to various microbial agents. We have previously shown
that human dermal endothelial cells (HMEC) express TLR4, but very
little TLR2, and respond to LPS, but not to Mycobacterium
tuberculosis 19-kDa lipoprotein, unless transfected with TLR2.
Here we report that HMEC are unresponsive to several additional
biologically relevant TLR2 ligands, including, phenol-soluble modulin
(PSM), a complex of three small secreted polypeptides from the skin
commensal Staphylococcus epidermidis, soluble
tuberculosis factor (STF), and Borrelia burgdorferi
outer surface protein A lipoprotein (OspA-L). Expression of TLR2
renders HMEC responsive to all these ligands. We further characterized
the signaling pathway in response to STF, OspA-L, and PSM in
TLR2-transfected HMEC. The TLR2 signaling pathway for NF-
B
trans-activation shares the IL-1R signaling molecules.
Dominant negative constructs of TLR2 or TLR6 inhibit the responses of
STF and OspA-L as well as PSM in TLR2-transfected HMEC, supporting the
concept of functional cooperation between TLR2 and TLR6 for all these
TLR2 ligands. Moreover, we show that Toll-interacting protein (Tollip)
coimmunoprecipitates with TLR2 and TLR4 using HEK 293 cells, and
overexpression of Tollip inhibits NF-B activation in response to
TLR2 and TLR4 signaling. Collectively, these findings suggest that
there is functional interaction between TLR2 and TLR6 in the cellular
response to STF and OspA-L in addition to S. epidermidis
(PSM) Ags, and that engagement of TLR2 triggers a signaling cascade,
which shares the IL-1R signaling molecules, similar to the TLR4-LPS
signaling cascade. Our data also suggest that Tollip may be an
important constituent of both the TLR2 and TLR4 signaling
pathways.
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G. Melmed, L. S. Thomas, N. Lee, S. Y. Tesfay, K. Lukasek, K. S. Michelsen, Y. Zhou, B. Hu, M. Arditi, and M. T. Abreu Human Intestinal Epithelial Cells Are Broadly Unresponsive to Toll-Like Receptor 2-Dependent Bacterial Ligands: Implications for Host-Microbial Interactions in the Gut J. Immunol., February 1, 2003; 170(3): 1406 - 1415. [Abstract] [Full Text] [PDF]
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H. Weighardt, S. Kaiser-Moor |
