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<p><i>N</i><sup>6</sup>-methyladenosine (m<sup>6</sup>A) is the most abundant internal modification of eukaryotic mRNA, and its dysregulation is increasingly linked to autoimmune diseases. Unlike previous reviews that broadly cover the entire m<sup>6</sup>A network, this review adopts an m<sup>6</sup>A writer centric perspective. The m<sup>6</sup>A writer complex serves as the upstream gatekeeper of epitranscriptomic regulation. We summarize its structural organization and cell‑type‑specific functions in controlling immune cell differentiation and function, as well as its protective roles in parenchymal tissues. Accumulating evidence shows that the writer complex exerts context‑dependent dual actions across a wide range of autoimmune conditions, including rheumatoid arthritis, lupus, psoriasis, and others. We also discuss the mechanistic basis of this functional heterogeneity, involving microenvironmental signals, subunit composition, and reader proteins. Notably, our review not only focuses on the roles and mechanisms of writer‑mediated m<sup>6</sup>A modification in various immune cells but also summarizes its pharmacological modulators, which represents a key advantage over previous reviews. By focusing specifically on the writer complex, we provide a more proximal and mechanistically feasible framework for precise epitranscriptomic intervention in autoimmune disorders.</p>

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RNA m6A methylation writers in autoimmune diseases: structure, function, and therapeutic opportunities

  • 期刊论文

  • 发表日期：

    2026年7月6日

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  • Xue-feng Gao,
  • Gao-na Shi,
  • Ya-nan Wang,
  • Bo Zhang,
  • Li Li,
  • Tian-tai Zhang

摘要

N6-methyladenosine (m6A) is the most abundant internal modification of eukaryotic mRNA, and its dysregulation is increasingly linked to autoimmune diseases. Unlike previous reviews that broadly cover the entire m6A network, this review adopts an m6A writer centric perspective. The m6A writer complex serves as the upstream gatekeeper of epitranscriptomic regulation. We summarize its structural organization and cell‑type‑specific functions in controlling immune cell differentiation and function, as well as its protective roles in parenchymal tissues. Accumulating evidence shows that the writer complex exerts context‑dependent dual actions across a wide range of autoimmune conditions, including rheumatoid arthritis, lupus, psoriasis, and others. We also discuss the mechanistic basis of this functional heterogeneity, involving microenvironmental signals, subunit composition, and reader proteins. Notably, our review not only focuses on the roles and mechanisms of writer‑mediated m6A modification in various immune cells but also summarizes its pharmacological modulators, which represents a key advantage over previous reviews. By focusing specifically on the writer complex, we provide a more proximal and mechanistically feasible framework for precise epitranscriptomic intervention in autoimmune disorders.