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<p>The regulation of IgA expression is crucial for maintaining mucosal immune homeostasis, providing a vital defense mechanism against pathogens at mucosal surfaces. However, the intricate mechanisms governing IgA class-switch recombination and its dysregulation in diseases such as inflammatory bowel disease remain a significant challenge in the field. Our study delves into the significance of IgA regulation in mucosal immunity, focusing on the <i>N</i><sup>4</sup>-acetylcytidine (ac<sup>4</sup>C) in NIK mRNA by NAT10 in B cells. We discovered that NAT10-mediated ac<sup>4</sup>C stabilizes NIK mRNA, thereby promoting IgA production, which is pivotal for immune defense. Our findings in a B-cell conditional NAT10 knockout mouse model highlight a reduction in IgA expression and a dampened noncanonical NF-κB pathway, suggesting NAT10 as a potential therapeutic target for IgA-related disorders. This research provides novel insights into the post-transcriptional regulation of IgA and underscores the role of NAT10 in modulating mucosal immunity.</p>

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NAT10-mediated acetylation of NIK mRNA in B cells promotes IgA production

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年7月4日

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  • Wan-Jun Jiang,
  • Xin-Tao Mao,
  • Wen-Ping Li,
  • Nicole Jin,
  • Yu Wang,
  • Guiping Guan,
  • Jin Jin,
  • Yi-Yuan Li

摘要

The regulation of IgA expression is crucial for maintaining mucosal immune homeostasis, providing a vital defense mechanism against pathogens at mucosal surfaces. However, the intricate mechanisms governing IgA class-switch recombination and its dysregulation in diseases such as inflammatory bowel disease remain a significant challenge in the field. Our study delves into the significance of IgA regulation in mucosal immunity, focusing on the N4-acetylcytidine (ac4C) in NIK mRNA by NAT10 in B cells. We discovered that NAT10-mediated ac4C stabilizes NIK mRNA, thereby promoting IgA production, which is pivotal for immune defense. Our findings in a B-cell conditional NAT10 knockout mouse model highlight a reduction in IgA expression and a dampened noncanonical NF-κB pathway, suggesting NAT10 as a potential therapeutic target for IgA-related disorders. This research provides novel insights into the post-transcriptional regulation of IgA and underscores the role of NAT10 in modulating mucosal immunity.