The human monocyte model BLaER1 exhibits an epigenetic GPI anchor defect that impairs TLR4 signaling. The human monocyte model BLaER1 exhibits an epigenetic GPI anchor defect that impairs TLR4 signaling

We show that the human monocyte model BLaER1 contains GPI-anchor-deficient cells, which lack CD14 surface expression when differentiated to monocytes, resulting in diminished LPS/TLR4 responsiveness. We found that this GPI anchor defect is caused by epigenetic silencing of the PIGH gene, leading to a random distribution of intact and PIGH-deficient clones after single-cell cloning. Overall design: Comparison of mRNA expression profiles of 3 undifferentiated GPI-positive and 4 undifferentiated GPI-negative BLaER1 monoclonal cell lines