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J Biol Chem, Vol. 275, Issue 13, 9773-9781, March 31, 2000
From the The protein product of the Toll-like receptor
(TLR) 4 gene has been implicated in the signal transduction events
induced by lipopolysaccharide (LPS). In mice, destructive mutations of
Tlr4 impede the normal response to LPS and cause a high
susceptibility to Gram-negative infection. Expression of TLR4 mRNA
in humans is restricted to a small number of cell types, including
LPS-responsive myeloid cells, B-cells, and endothelial cells. To
investigate the molecular basis for TLR4 expression in cells of myeloid
origin, we cloned the human TLR4 gene and analyzed its putative
5'-proximal promoter. In transient transfections a region of only 75 base pairs upstream of the major transcription initiation site was sufficient to induce maximal luciferase activity in THP-1 cells. The
sequence of this region is similar in human and mouse TLR4 genes and
lacks a TATA box, typical Sp1-sites or CCAAT box sequences. Instead, it
contains consensus-binding sites for Ets family transcription factors,
octamer-binding factors, and a composite interferon response factor/Ets
motif. The activity of the promoter in macrophages was strictly
dependent on the integrity of both half sites of the composite
interferon response factor/Ets motif, which was constitutively bound by
the myeloid and B-cell-specific transcription factor PU.1 and
interferon consensus sequence-binding protein. These results indicate
that the two tissue-restricted transcription factors PU.1 and
interferon consensus sequence-binding protein participate in the basal
regulation of human TLR4 in myeloid cells. Cloning of the human TLR4
gene provides a basis for further investigation of the possible impact
of genetic variations on the susceptibility to infection and sepsis.
PU.1 and Interferon Consensus Sequence-binding Protein Regulate
the Myeloid Expression of the Human Toll-like Receptor 4 Gene*
§,,,, and
**
Department of Hematology and Oncology,
University of Regensburg, 93042 Regensburg, Germany, and Howard
Hughes Medical Institute and the ¶ Department of Internal
Medicine, University of Texas Southwestern Medical Center,
Dallas, Texas 75235-9050
*
This work was supported by a grant from the University of
Regensburg (to M. R.).The costs of publication of this
article were defrayed in part by the
payment of page charges. The article
must therefore be hereby marked
"advertisement" in
accordance with 18 U.S.C. Section
1734 solely to indicate this fact.
Copyright © 2000 by The American Society for Biochemistry and Molecular Biology, Inc.
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E. Faure, L. Thomas, H. Xu, A. E. Medvedev, O. Equils, and M. Arditi Bacterial Lipopolysaccharide and IFN-{{gamma}} Induce Toll-Like Receptor 2 and Toll-Like Receptor 4 Expression in Human Endothelial Cells: Role of NF-{{kappa}}B Activation J. Immunol., February 1, 2001; 166(3): 2018 - 2024. [Abstract] [Full Text] [PDF]
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