GEOapplication/xmlftp://ftp.ncbi.nlm.nih.gov/geo/series/GSE266nnn/GSE266417/primaryOK200TranscriptomicsMus musculusExpression profiling by high throughput sequencinghttps://www.ncbi.nlm.nih.gov/geo/query/acc.cgi?acc=GSE266417GEOGSEfalseFemale 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.2026/05/15GSE266417GSM8246649GSM8246669GSM8246647GSM8246648GSM8246667GSM8246645GSM8246668GSM8246646GSM8246665GSM8246666GSM8246644GSM8246663GSM8246664GSM8246661GSM8246662GSM8246660GSM8246658GSM8246659GSM8246656GSM8246657GSM8246654GSM8246655GSM8246652GSM8246653GSM8246650GSM8246651GSM8246670GSM824667130172266417Mus musculus