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. 2008 Apr 21;9:39. doi: 10.1186/1471-2199-9-39

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Copyright © 2008 Furuta et al; licensee BioMed Central Ltd.

This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

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A potential model representing the mechanisms underlying hypomethylation-dependent TLR2 promoter activation in human epithelial cells. Enhanced methylation of the CpG#18-20 site within TLR2 promoter observed in non-CF epithelial cells is followed by the enhanced recruitment of unknown factors "X" that could recognize methylated CpGs and could suppress SP1-dependent transcriptional activation without affecting the binding of SP1 to those CpGs (left panel). 5-azacytidine (5-AC) treatment of non-CF cells leads to the demethylation of CpG#18-20. On the other hand, CF epithelial cells express high level of TLR2 gene through decreased methylation of CpG#18-20, which might abolish the recruitment and activity of factors "X" in these cells (right panel).