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CUTTING EDGE |
,§
*
Department of Biochemistry, Hyogo College of Medicine, Hyogo, Japan;
Research Institute, International Medical Center of Japan, Tokyo, Japan;
Department of Oral Microbiology, Asahi University School of Dentistry, Gifu, Japan; and
§
Core Research for Evolutional Science and Technology, Japan Science and Technology Corporation, Japan.
The human homologue of Drosophila Toll (hToll),
also called Toll-like receptor 4 (TLR4), is a recently cloned receptor
of the IL-1/Toll receptor family. Interestingly, the TLR4 gene has been
localized to the same region to which the Lps locus
(endotoxin unresponsive gene locus) is mapped. To examine the role of
TLR4 in LPS responsiveness, we have generated mice lacking TLR4.
Macrophages and B cells from TLR4-deficient mice did not respond to
LPS. All these manifestations were quite similar to those of
LPS-hyporesponsive C3H/HeJ mice. Furthermore, C3H/HeJ mice have, in the
cytoplasmic portion of TLR4, a single point mutation of the amino acid
that is highly conserved among the IL-1/Toll receptor family.
Overexpression of wild-type TLR4 but not the mutant TLR4 from C3H/HeJ
mice activated NF-
B. Taken together, the present study demonstrates
that TLR4 is the gene product that regulates LPS
response.
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