The authors identified an important caveat when investigating TLR4-driven signaling in BLaER1 cells. They showed that this model contained glycosylphosphatidylinositol anchor-deficient cells, which lacked CD14 surface expression when differentiated to monocytes, resulting in diminished LPS/TLR4 but not TLR7/TLR8 responsiveness.
[Scientific Reports]
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Wegner, J., Zillinger, T., Schlee-Guimaraes, T., Bartok, E., & Schlee, M. (2021). An epigenetic GPI anchor defect impairs TLR4 signaling in the B cell transdifferentiation model for primary human monocytes BLaER1. Scientific Reports, 11(1), 14983. https://doi.org/10.1038/s41598-021-94386-z Cite
