Abstract
The imbalance of sex chromosomes between females (XX) and males (XY) necessitates strict regulation of X-linked gene expression. X-Chromosome Inactivation (XCI) selects one X for transcriptional silencing in the early embryo, generating an epigenetically distinct and transcriptionally silent X that is maintained into adulthood. Some genes on the inactive X escape XCI, and human somatic cells have a greater number of escape genes compared to mice. Advances with single-cell technologies have revealed human-specific escape genes in fibroblasts and immune cells, some of which exhibit cell and tissue specificity. Here, we review recent discoveries of dynamic XCI in female immune cells, which have changed our understanding of XCI maintenance, and discuss how some X-linked genes might become overexpressed in female-biased autoimmunity.