GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE266nnn/GSE266231/primaryOK200TranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE266231GEOGSEfalseFemale Mice with an Xist Deletion in B Cells Can Develop Lupus-Associated PhenotypesSystemic lupus erythematosus (SLE) is a female-biased autoimmune disease. X-Chromosome Inactivation (XCI) dosage compensates X-linked genes in females. Disrupted localization of Xist, a critical regulator of XCI, and aberrant expression of X-linked genes in female SLE patients and SLE mouse models suggest that XCI impairment contributes to disease. To test this, we conditionally deleted Xist in B cells (Xist cKO mice). Remarkably, some female Xist cKO mice spontaneously develop SLE phenotypes, including expansion of activated B cell subsets, development of disease-associated autoantibodies, and glomerulonephritis. Moreover, female Xist cKO mice with chemically induced SLE developed more activated B cells and dsDNA autoantibodies compared to treated wildtype female mice. Activated B cells from Xist cKO mice with SLE phenotypes have increased expression of X-linked immunity genes implicated in female-biased SLE. Our findings demonstrate that perturbations in B cell XCI maintenance directly contribute to female-biased SLE via upregulation of X-linked immunity-related genes.2026/05/15GSE266231GSM8242717GSM8242718GSM8242719GSM8242713GSM8242714GSM8242715GSM8242716GSM8242720GSM8242721GSM8242722GSM8242723GSM8242706GSM8242728GSM8242729GSM8242707GSM8242708GSM8242709GSM8242724GSM8242703GSM8242725GSM8242726GSM8242704GSM8242727GSM8242705GSM8242731GSM8242732GSM8242710GSM8242733GSM8242711GSM8242734GSM8242712GSM824273030172266231Mus musculus