TLR8 escapes X chromosome inactivation in human monocytes and CD4 + T cells.
Ali YounessClaire CénacBerenice Faz-LópezSolange GrunenwaldFranck J BarratJulie ChaumeilJosé Enrique MejiaJean-Charles GuéryPublished in: Biology of sex differences (2023)
T cells. Co-dependent transcription from the active X chromosome and escape from XCI could both contribute to higher TLR8 protein abundance in female cells, which may have implications for the response to viruses and bacteria, and the risk of developing inflammatory and autoimmune diseases.
Keyphrases
- toll like receptor
- inflammatory response
- induced apoptosis
- immune response
- endothelial cells
- copy number
- cell cycle arrest
- oxidative stress
- nuclear factor
- transcription factor
- induced pluripotent stem cells
- endoplasmic reticulum stress
- peripheral blood
- signaling pathway
- gene expression
- binding protein
- small molecule
- amino acid
- dna methylation
- pi k akt