Abstract

Sexual dimorphism contributes to autoimmune diseases, such as systemic lupus erythematosus (SLE), where the female-to-male ratio is 9:1. Although hormonal and sex chromosome variation contribute to women being more prone to such diseases, the predominant driving mechanism(s) remain unknown. We hypothesize that male and female keratinocytes display distinct differences in chromatin landscape and nucleosome accessibility that enforce differences in inflammatory responses. We have assessed chromatin landscape differences by performing assay for transposase accessibility sequencing (ATAC-seq) on primary keratinocytes (KCs) isolated from healthy male and female donors (n=3, each).

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