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<p>A strong female bias is characteristic of systemic lupus erythematosus (SLE), the prototypic systemic autoimmune disease. Here, through an unbiased transcriptome analysis, we report a pronounced female-biased expression of the cohesin complex subunit <i>SMC1A</i>, a genome architectural factor, in monocytes from SLE patients compared to those from healthy individuals or patients with ankylosing spondylitis, a non-sex-biased autoimmune disorder. Integration of SMC1A binding, chromatin activity, and accessibility in lupus-like monocytes reveals extensive SMC1A redistribution to active enhancers of immune/inflammatory genes, inducing their transcription. SLE monocyte transcriptomes demonstrate significant enrichment of female-biased immune/inflammatory genes among SMC1A targets, accompanied by increased secretion of cytokines including IL6, with enhanced SMC1A binding at their enhancers in lupus-like monocytes. Collectively, our study highlights <i>SMC1A</i> as a female-biased chromatin modifier that acquires a specific regulatory function during lupus, accentuating inflammatory pathways and providing mechanistic insights into the female-biased predisposition to SLE and other autoimmune diseases.</p>

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The sex-biased chromatin modifier SMC1A promotes autoimmunity by shaping inflammatory pathways in patients with SLE

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年11月24日

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  • Despoina Kosmara,
  • Sofia Papanikolaou,
  • Chrysoula Stathopoulou,
  • Dionysios Papamatheakis,
  • Giannis Vatsellas,
  • Arianna Cimmarrusti,
  • Aggelos Banos,
  • Prodromos Sidiropoulos,
  • Matthieu D. Lavigne,
  • Panayotis Verginis,
  • Dimitrios Boumpas,
  • Charalampos Spilianakis,
  • Dimitris Konstantopoulos,
  • Christoforos Nikolaou,
  • George Bertsias

摘要

A strong female bias is characteristic of systemic lupus erythematosus (SLE), the prototypic systemic autoimmune disease. Here, through an unbiased transcriptome analysis, we report a pronounced female-biased expression of the cohesin complex subunit SMC1A, a genome architectural factor, in monocytes from SLE patients compared to those from healthy individuals or patients with ankylosing spondylitis, a non-sex-biased autoimmune disorder. Integration of SMC1A binding, chromatin activity, and accessibility in lupus-like monocytes reveals extensive SMC1A redistribution to active enhancers of immune/inflammatory genes, inducing their transcription. SLE monocyte transcriptomes demonstrate significant enrichment of female-biased immune/inflammatory genes among SMC1A targets, accompanied by increased secretion of cytokines including IL6, with enhanced SMC1A binding at their enhancers in lupus-like monocytes. Collectively, our study highlights SMC1A as a female-biased chromatin modifier that acquires a specific regulatory function during lupus, accentuating inflammatory pathways and providing mechanistic insights into the female-biased predisposition to SLE and other autoimmune diseases.