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<p>Interleukin-6 (IL-6) drives metabolic and inflammatory processes central to disease. Current knowledge implicates epigenetic mechanisms in the regulation of these pathways, including through the methylation of CpG sites. This blood-based meta-analysis of three cohorts (n = 4,361) identifies 401 IL-6–associated CpGs enriched in regulatory regions and linked to key immunometabolic genes, including <i>AIM2</i>, <i>MTOR</i>, and <i>IL6R</i>. Three complementary causal inference approaches support most sites as responding to IL-6, with <i>SOCS3</i> (Suppressor of Cytokine Signalling 3) methylation statistically mediating inflammatory bowel disease risk. Notably, one CpG connected to <i>NFATC2IP</i> (Nuclear Factor of Activated T-cells 2 Interacting Protein) plausibly influences both IL-6 production and multiple immunometabolic conditions, including body mass index and type 2 diabetes. Collectively, our results map the DNA methylation landscape surrounding circulating IL-6 levels and unveil directional effects and distinct functional relationships between epigenetics and inflammation.</p><p></p>

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Epigenome-wide association study of circulating interleukin-6 connects DNA methylation to immunometabolic and inflammatory health

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2026年2月4日

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  • Lucy Sinke,
  • Jenny van Dongen,
  • Thomas Delerue,
  • Rory Wilson,
  • Yujing Xia,
  • Marian Beekman,
  • Gonneke Willemsen,
  • Christian Gieger,
  • Christian Herder,
  • Wolfgang Koenig,
  • Annette Peters,
  • Eco J. C. de Geus,
  • José M. Ordovas,
  • Jordana T. Bell,
  • Melanie Waldenberger,
  • Dorret I. Boomsma,
  • P. Eline Slagboom,
  • Bastiaan T. Heijmans

摘要

Interleukin-6 (IL-6) drives metabolic and inflammatory processes central to disease. Current knowledge implicates epigenetic mechanisms in the regulation of these pathways, including through the methylation of CpG sites. This blood-based meta-analysis of three cohorts (n = 4,361) identifies 401 IL-6–associated CpGs enriched in regulatory regions and linked to key immunometabolic genes, including AIM2, MTOR, and IL6R. Three complementary causal inference approaches support most sites as responding to IL-6, with SOCS3 (Suppressor of Cytokine Signalling 3) methylation statistically mediating inflammatory bowel disease risk. Notably, one CpG connected to NFATC2IP (Nuclear Factor of Activated T-cells 2 Interacting Protein) plausibly influences both IL-6 production and multiple immunometabolic conditions, including body mass index and type 2 diabetes. Collectively, our results map the DNA methylation landscape surrounding circulating IL-6 levels and unveil directional effects and distinct functional relationships between epigenetics and inflammation.